Twenty Six Annotated Bibliographies

Castellana, M., Hsin-Jung Li, S., & Wingreen, N. S. (2016, August 16). Spatial

organization of bacterial transcription and translation. Retrieved from

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4995950/

In order to understand how genetic disorders impact the physical phenotype of an

organism, one must understand the mechanisms in which DNA forms the phenotypic expression

of an organism. The mechanisms in which this happens are called transcription and translation.

To begin, DNA is kept and secured in the nucleus of a eukaryotic cell. When transcription

begins, helicase acts on the DNA to unzip the double helix shape and form two single helix

structures. After this has been completed, RNA polymerase acts on one unzipped DNA strand to

produce mRNA that possesses opposite base pairs to the DNA. For example, if DNA possesses

an Adenine base, mRNA will produce a uracil base. After the mRNA produces opposite base

pairs for the whole strand of DNA, it exits the nucleus and moves towards the membrane bound

ribosomes located in the rough endoplasmic reticulum. This is the site in which translation

occurs. When translation begins, the mRNA strand binds to a ribosome that is attached to tRNA.

The tRNA possesses anticodons that form codons, which consist of three base pairs, on the

mRNA. After the mRNA codons have been formed, tRNA attaches different amino acids to the

codons depending on what base pairs the codons consist of. tRNA attaches an amino acid for

every codon on the mRNA strand. After this is done, the amino acids gather together to form

proteins. The expression of these proteins is what makes and alters the phenotype of an

organism.
 The first author, Michele Castellana, is qualified to discuss genetic expression because

his credentials or experience includes being a member of the Institute for Integrative Genomics,

being a member of the Physical Chemistry Curie Institute, and publishing other related scholarly

articles like an article by the name of Enzyme clustering accelerates processing of intermediates

through metabolic channeling. The author’s contact information is not included in the article but

can be found with further research. The second author, Sophia Hsin-Jung Li, is qualified to

discuss genetic expression because her credentials or experience includes being a member of

Princeton’s Department of Molecular biology and publishing other related scholarly articles like

an article by the name of Human SHMT inhibitors reveal defective glycine import as a targetable

metabolic vulnerability of diffuse large B-cell lymphoma. This author’s contact information is

not included in the article but can be found with further research. The third author, Ned S.

Wingreen, is qualified to discuss genetic expression because his credentials or experience

includes being a member of the Lewis-Sigler Institute for Integrative Genomics and publishing

other related scholarly articles like an article by the name of Established Microbial Colonies Can

Survive Type VI Secretion Assault. The author’s contact information is not included in the

article but can be found with further research. This article was written 3 years ago and is current

on the topic of science. The authors thoroughly evaluated all sides of the issue. For example,

they acknowledge that RNA localization is hard to prove and then addressed that opposing

viewpoint by saying certain bacteria expressed the localization of mRNA. This inclusion shows

that all viewpoints were acknowledged. The coverage can be considered broad and deep because

the article describes all of transcription and translation but goes into specifics with mRNA

localization. The information contained in the source can be verified elsewhere. For example, the

author says that mRNA is involved in protein synthesis. This can be corroborated by an article
by the name of The protein-coding region of c-myc. This article states mRNA contains a

sequence that induces protein synthesis, which means mRNA affects translation because

translation is the production of proteins. The purpose of this article is to inform and educate the

audience. The audience is researchers and geneticists. The article is appropriate for this purpose

and audience because the article contains complex ideas and terminology. For example, the

article uses terms like RNA localization nucleoid segregation.

 Harper, C. B., & Cousin, M. A. (2017, September 5). Altered synaptobrevin-II trafficking

in neurons expressing a synaptophysin mutation associated with a severe

neurodevelopmental disorder. Retrieved from

https://www.sciencedirect.com/science/article/pii/S0969996117302103

Genetic disorders derive from mutations in the genetic coding of an organism. Different

types of genetic disorders are created by different types of mutations. One category of mutation

is point shift mutation. Point shift mutations are changes to a particular base pair. Within the

point shift mutation category, there are two different types of mutations. Transition and

transversion mutations. Transition mutations are changes of one base pair to another. For

example, in DNA, if an Adenine base pair mutated to a Guanine base pair, that would be

considered a transition mutation. Transition mutations can be harmful for the following reason.

During transcription and translation, DNA is transcripted to mRNA, and mRNA is translated into

amino acids which form proteins that impact the phenotypic expression of an organism. An

altered DNA base pair results in an altered mRNA base pair. An altered mRNA base pair results

in an altered codon. An altered codon results in the production of another Amino acid. Another

amino acid produces a slightly different protein which could disrupt the homeostasis within an

organism. This could kill or negatively impact the organism. Transversion mutations are

switches in one base pair and its corresponding base pair on the other strand of the DNA

molecule. For example, in DNA, if there is Adenine on strand 1 and Thymine on strand 2, a

transversion mutation would cause Thymine to appear on stand 1 and Adenine to appear on stand

2 in the exact same location. Transversion mutations could be harmful for the following reason.

One strand of DNA transcribes to one strand of mRNA. One strand of mRNA translates to an
amino acid. Amino acids form proteins. Proteins form phenotypes. If the bases are switched on

the two strands of DNA, one strand is going to possess an incorrect base pair. This creates

mRNA with one incorrect base pair. This results in the production of an incorrect amino acid.

This results in the formation of an incorrect protein. This could disrupt the homeostasis of an

organism due to the lack of the correct protein and the presence of the new protein. Both

transversion and transition mutations are the cause for multiple disorders and diseases.

The first author, Callista B.Harper, is qualified to discuss genetics and mutations

because her credentials and experience includes being a member of the Center for Integrative

Physiology at the University of Edinburgh and publicizing scholarly articles like sdTIM is a

single-molecule technique for dissecting heterogeneous motion states of subdiffractional

endocytic compartments in live neurons. Her contact information is not included in the article

but can be found with further research. The second author, Michael A.Cousin, is qualified to

discuss genetics and mutations because his credentials and experience includes being a member

of the Center for Integrative Physiology at the University of Edinburgh and publicizing scholarly

articles like Building a better dynasore: the dyngo compounds potently inhibits dynamin and

endocytosis. His contact information is included in the article. This article was written 2 years

and is current on the topic of the sciences. Even though this is an opinion, the authors still

present claims, reasoning, and evidence to show why that opinion is valid and credible. For

example, the authors stated that the SV point mutation had no effect on phenotype. The authors

presented evidence for this claim by stating markers within the altered base pair did not appear

on the produced protein. The coverage can be considered broad and deep because the article

described all the types of point mutations and goes into specifics about each type. The

information contained in the source can be verified elsewhere. For example, the author says that
point mutations causing altered transmission of information between neurons cause neurological

disorders. This can be corroborated by Early synaptic pathophysiology in neurodegeneration:

insights from Huntington's disease. In this publication, it is stated that neurological disorders are

caused by Hungtinson’s disease. The disease causes dysfunctions in the transmission of

information between neurons due to point mutations. The purpose of this article is to inform and

educate the audience. The audience is genetic researchers and geneticists. The article is

appropriate for this purpose and audience because it contains ideas that have been built off

background knowledge the audience should have. For example, the article presents transition and

transversion mutations as the cause for altered information transmission in genetic disorders. The

author is assuming the audience understands how transition and transversion mutations work and

alter phenotype in order to state that transition and transversion mutations cause altered

information transmission.
 Anderson1, B., Epstein1, A., Hodgetts2, S., Leonard1, H., & Downs1, J. (2016, April

14). Prevalence and onset of comorbidities in the CDKL5 disorder differ from Rett

syndrome. Retrieved from https://ojrd.biomedcentral.com/articles/10.1186/s13023-016-

0418-y

Mutations in the genetic coding of an organism can cause genetic disorders. One category

of mutations are frameshift mutations. Frameshift mutations are changes in the amount of base

pairs within a strain of DNA. There are two different types of frameshift mutations. The first

type is insertion mutations. In this mutation, base pairs are added to a DNA strand. This type of

mutation is very damaging due to the following reason. During transcription and translation,

DNA becomes mRNA, mRNA codons (3 base pairs each) become amino acids, and amino acids

become proteins. If base pairs are added to DNA, each codon of mRNA changes as the base

pairs on the mRNA shifts. This causes each amino acid to change. This results in the protein

changing in entirety as well. This is much more damaging than point shift mutations as they only

impact one amino acid. Organisms are more likely to experience death and more debilitating

disorders with insertion mutations. The second type of frameshift mutation is a deletion

mutation. In this mutation, base pairs are removed from a DNA strand. This results in the same

effect as insertion mutation as it comes to protein synthesis.

The first author, Meghana Mangatt, is qualified to discuss genetics and mutations because

her credentials and experience includes being a member of the School of Anatomy, Physiology,

and Human Biology at the University of Western Australia. Her contact information is not

included in the article but can be found with further research. The second author, Helen Leonard,

is qualified to discuss genetics and mutations because her credentials and experience include
being an Associate Professor at Telethon kids institute in which she heads the child disability

unit and publicizing scholarly articles like Effects of MECP2 mutation type, location and X‐

inactivation in modulating Rett syndrome phenotype. Her contact information is included in the

article. The article was written 3 years ago. This source is current on the topic of the sciences.

Even though this is an opinion, the author still presents claims, reasoning, and evidence to show

why that opinion is valid and credible. For example, the authors claim that CDLK5’s symptoms

get worse as an organism ages. This is supported with evidence from the experiment and

scientific knowledge about frameshift mutations and how they negatively impact an individual as

they get older. The coverage can be considered broad and deep because the authors go over all of

the different frameshift mutations but gogoes in depth about each mutation. The information

contained in the source can be verified elsewhere. For example, the authors say that mutation in

the CDKL5 gene were spotted in children with West syndrome. This can be corroborated by an

article by the name of CDKL5 disruption by t(X;18) in a girl with West syndrome. In this

publication, it is stated that a girl with West syndrome had a mutation in the CDKL5 gene. The

purpose of this article is to educate and inform the audience. The audience is genetic researchers

and geneticists. The article is appropriate for this purpose and audience because of the complex

ideas and terminology. For example, the article uses words like catalytic domain and active

region.
 Li, L., & Petrovsky, N. (1970, January 1). Molecular mechanisms for enhanced DNA

vaccine immunogenicity. Retrieved from https://europepmc.org/articles/pmc4955855

The use of plasmids have been thought of as a possible solution to certain disorders.

Plasmids are vesicles with circular pieces of DNA within them. They are gotten by extracting the

prokaryotic DNA within the cytoplasm of a bacteria. The circular piece of DNA can be altered

by directly altering the bacteria the DNA is gotten from or deleting and inserting new slices of

DNA from other bacterial organisms. Through these two processes, plasmids are highly

customizable with wanted pieces of DNA from different bacterial organisms being able to be

added to the circular piece of DNA within the plasmid. After being altered, plasmids can be

inserted into the bacteria and add their genetic coding to the DNA of the bacteria. This results in

the transcription and translation of the new pieces of DNA into mRNA, amino acids, and

ultimately new proteins which affect the phenotype of the bacteria. By having the plasmid

interact with the bacteria, the bacteria would now express a new phenotype depending on the

DNA within the plasmid. Now, plasmids have begun being thought of as a possible solution to

certain disorder by applying them to human eukaryotic cells. By inserting plasmids into the

nucleus of a eukaryotic cell, new DNA can be added to the existing DNA. This will lead to new

phenotypic expression. This new phenotypic expression can benefit the organism if the plasmid

contains DNA that codes for proteins that might disrupt the proteins produced as a result of the

disorder.

The first author, Lei Li, is qualified to discuss genetics and plasmids because

his credentials and experience include being a member of the Department of Endocrinology at

Flinders university and publicizing other scholarly articles like Defining the specificity space of
the human SRC homology 2 domain. His contact information is not included in the article but

can be found with further research. The second author, Nikolai Petrovsky, is qualified to discuss

genetics and plasmids because his credentials and experience include being the director of the

Department of Endocrinology at Flinders university and publicizing other scholarly articles like

Adjuvant Strategies for More Effective Tuberculosis Vaccine Immunity. His contact information

is not included in the article but can be found with further research. This source was written 4

years ago. This source is current on the topic of the sciences. The author thoroughly evaluated all

sides of the issue. For example, when the author states DNA vaccines have fallen short when

used on humans, he brings up the use of not only plasmids but also codon optimization,

electroporation, and gene transfection. The coverage can be considered broad because the

authors describe everything about plasmids including how they’re developed, how they’re

altered, how they work, and how they’re used. The coverage can be considered deep because the

authors go into specifics about the mechanisms in which plasmids impact the phenotypic

expression of cells. The information contained in the source can be verified elsewhere. For

example, the author says the first DNA vaccine involved RNA and DNA vectors. This can be

corroborated by an article by the name of Direct gene transfer into mouse muscle in vivo. In this

publication, it is stated that RNA and DNA expression vectors were used as a DNA vaccination

to vaccinate organisms. The purpose of this article is to inform and educate the audience. The

audience is researchers and geneticists. The article is appropriate for this purpose and audience

because it contains complex ideas and terminology. For example, terms like DNA vector boost

and immunogenicity are used.

 McIntosh, J. R. (2016, September). Mitosis. Retrieved from

https://europepmc.org/articles/pmc5008068

Mitosis occurs in every multicellular organism. During mitosis, mutation is rare but

possible and may result in the development of a disorder. Mitosis is a multistep process

consisting of interphase, prophase, metaphase, anaphase, telophase, and cytokinesis. Before

interphase, the cell is fully developed and possesses the full array of chromosomes. During

interphase, the chromosomes begin to untangle and distinctify, and the centrosomes begin to

form on one edge of the cell. Interphase is getting the cell ready for the following steps of

mitosis. After interphase, during prophase, each untangled chromosome gets duplicated, and

there are double the amount of chromosomes as there were before interphase. This is when

mutation can occur. The individual sister chromatids now form an x like structure with their

copies. The centrosomes begin to move, so they are at opposite ends of the nucleus. After

prophase, during metaphase, spindle fibers, which are made of proteins, form on the centrosomes

to get ready to pull the chromosomes to the sides each centrosome is at. The nucleus that was

previously encapsulating the chromosomes disappears, and the chromosomes drift to the middle

of the cell. After metaphase, during anaphase, the spindle fibers start dragging a sister chromatid

from each chromosome to their side. After this has been completed, telophase begins. In

telophase, the cell wall begins to split. Two new nuclei form on each side of the cell to

encapsulate the chromosomes on each side. Eventually, the cell splits into two cells with each

cell containing the exact same DNA as the original cell.

The author, Richard J. McIntosh, is qualified to discuss genetics and mitosis because his

credentials and experience include being a member of the Department of Molecular, Cellular,
and Developmental Biology at the University of Colorado and publicizing other scholarly

articles like Computer Visualization of Three-Dimensional Image Data Using IMOD. His

contact information is included in the article. This article was written 3 years ago. This source is

current on the topic of the sciences. The author thoroughly evaluated all sides of the issue. For

example, when describing the mitotic spindle machine, the author discussed not only the use of

MT dynamics but also motor enzymes, proteins, and the cell wall. The coverage can be

considered broad because the author addresses all phases of mitosis. The coverage can be

considered deep because the author analyzes and explains each portion of each phase. The

information contained in the source can be verified elsewhere. For example, the author says all

eukaryotic cells form spindle fibers in preparation for mitosis. This can be corroborated by an

article by the name of The spindle: a dynamic assembly of microtubules and motors. In this

publication, it is stated that spindles are in each eukaryote and serve functions in mitosis. The

purpose of this article is to inform and educate the audience. The audience is researchers and

biologists. The article is appropriate for this purpose and audience because it contains complex

ideas and terminology. For example, ideas such as acute segregation and diploid chromosomes

are discussed.
 Zickler, D., & Kleckner, N. (2015, June). Recombination, Pairing, and Synapsis

of Homologs during Meiosis. Retrieved from https://europepmc.org/articles/pmc4448610

Meiosis is a process that occurs in every organism that goes through sexual reproduction.

Mutation is possible during certain steps of meiosis. Mutation in meiosis may lead to a disorder

in the organism. In Meiosis, there is Meiosis 1 and Meiosis 2. Beginning with Meiosis 1, there is

prophase 1, metaphase 1, anaphase 1, telophase 1, and cytokinesis. Meiosis 1 is similar but

different to mitosis. Before prophase 1, two gametes containing half of an organism’s

chromosomes interact. This results in the creation of a cell that begins with all of its DNA. After

this cell is developed, prophase 1 begins. During prophase 1, centrosomes form on the edge of

the cell, and DNA is untangled. When the DNA is untangled, some of the chromosomes

exchange genes with other chromosomes in an event called recombination or independent

assortment. During this event, there could be malfunctions, and mutations may ensue. After this

occurs, metaphase 1 will follow. During metaphase 1, the nucleus disappears, the chromosomes

float towards the middle of the cell, and spindle fibers appear on the centrosomes. After

metaphase 1, during anaphase 1, the spindle fibers grab whole chromosomes instead of sister

chromatids(like in mitosis) to each side. After this occurs, telophase 1 ensues. During this

process, the cell wall begins to contort to look like two cell walls, two nuclei form to encapsulate

the DNA , and centromeres disappear. During cytokinesis, the cells finally separate. These cells

contain half of the DNA of the original cell. After this is over, meiosis 2 follows. Meiosis 2 will

follow the same format as meiosis 1 except there will be no independent assortment and the cells

at the end of meiosis 1 will have one fourth of the DNA of the original cell.

The first author, Denise Zickler, is qualified to discuss genetics and meiosis because
her credentials include being a member of the Institute of Genetics and Microbiology at

Université Paris-Sud. Her contact information is included in the article. The second author,

Nancy Kleckner, is qualified to discuss genetics and meiosis because her credentials include

being a member of the Department of Molecular and Cellular Biology at Harvard University.

Her contact information is also included in the article. This article was written 3 years ago. This

source is current on the topic of the sciences. The authors thoroughly evaluated all sides of the

issue. For example, when describing recombination, the authors point out not only how

recombination increases genetic diversity in a population but also how it solves homologous

chromosomes being paired together and spatial problems. The coverage can be considered broad

because the author goes over all of the phases of meiosis I and II. The coverage can be

considered deep because the author analyzes each phase of meiosis I and II carefully. The

information contained in the source can be verified elsewhere. For example, the author says

recombination increases genetic diversity. This can be corroborated by an article by the name of

Direct and indirect consequences of meiotic recombination: implications for genome evolution.

In this publication, it is stated that recombination increased the rate of mutation in a population.

Mutation in a population increases the genetic diversity. The purpose of this article is to educate

and inform the audience. The audience is researchers and biologists. The article is appropriate for

this purpose and audience because convoluted terms and ideas are used. For example, words like

regular segregation and homologs are used.

 Watford, S., & Warrington, S. J. (2019, April 27). Bacterial DNA Mutations. Retrieved

from https://www.ncbi.nlm.nih.gov/books/NBK459274/

Disorders originate from mutations in the DNA of an organism. In order to understand

disorders, DNA must be understood. DNA is composed of nucleic acid and is the genetic

material for all modern day eukaryotic cells. DNA is used over RNA as DNA possesses a double

helix shape. RNA possesses a single helix shape meaning it is more prone to errors when

replicating. In an organism, all the genetic materials are either exons or introns. Most of the

genetic materials are introns, meaning they do not code for any proteins and therefore do not

impact the organism. A small portion of the genetic materials are exons, meaning they do code

for proteins and impact the organism. Mutations in DNA that is intronic has no effect on the

organism while mutations on DNA that is exonic has an effect on the organism. Introns and

exons work based on the composition of operons. Operons are composed of promoters,

operators, and genes. Promoters possesses RNA polymerase which transcribes the genetic

information into mRNA. This mRNA would then go to ribosomes to eventually synthesize

proteins. Operators can, however, possess regulatory proteins which prevent the RNA

polymerase from transcribing the genetic information into mRNA. Operons with operators that

possess regulatory proteins are introns. Operons with operators that do not possess regulatory

proteins are exons. Chromosomes consist of many of these operons.

The first author, Shelby Watford, is qualified to discuss genetics and DNA because

her credentials and experience include her position as an Emergency Medical Technician. Her

contact information is not included in the article but can be found with further research. The

second author, Steven J. Warrington, is qualified to discuss genetics and DNA because his
credentials and experience include being a doctor specializing in emergency medicine. His

contact information is not included in the article but can be found with further research. This

article was written 4 months ago. This source is current on the topic of the sciences. The authors

thoroughly evaluated all sides of the issue. For example, when the author describes mutations in

bacterial populations, they do not only mention how it may lead to dysfunction but also mention

how it may bring positive genetic variation to a population. The coverage can be considered

broad because the article mentions nearly everything about DNA. The coverage can be

considered deep because the article analyzes each component of DNA and its benefits. The

information contained in the source can be verified elsewhere. For example, the author says the

genetic material of bacteria is single stranded, circular, and double helixed. This can be

corroborated by an article by the name of Type II DNA topoisomerases: enzymes that can

unknot a topologically knotted DNA molecule via a reversible double-strand break. In this

publication, it is stated that the bacteria possesses a double stranded circular piece of DNA. The

purpose of this article is to educate and inform the audience. The audience is geneticists,

biologists, and researchers. The article is appropriate for this purpose and audience because it

provides essential information through convoluted terminology. For example, the article

describes operons, an essential part of the chromosome, with words like structural genes and

transcription factors.
 DiFrancesco, J. C., & DiFrancesco, D. (2015, February 18). Dysfunctional HCN ion

channels in neurological diseases. Retrieved from

https://www.frontiersin.org/articles/10.3389/fncel.2015.00071/full

Depolarization, repolarization, and hyperpolarization are processes that take place among

neurons. Most neurological diseases and disorders involve some malfunction in one of these. The

neuron possesses a large amount of positively charged potassium ions and a small amount of

positively charged sodium ions. The environment a neuron is in is the opposite. Depolarization is

the process a neuron goes through when there is a large enough stimulation. When there is a

stimulation, the sodium channels open, and positively charged sodium ions enter the atom. This

raises the voltage of the neuron until a certain point. At this point, the neuron is so positively

charged, it begins to go through repolarization. In repolarization, the sodium ion channels close,

and the potassium ion channels open. This results in potassium exiting the neuron and the neuron

lowering in voltage. This keeps going until the neuron becomes very slightly positively charged.

At this point, hyperpolarization occurs. The potassium ion channel closes, and the potassium

sodium channel begins increasing the voltage of the neuron slightly. This process keeps

occurring along the axon until the process reaches the dendrites. When it reaches the dendrites,

neurotransmitters are emitted and transfer to the next neuron. The process then repeats itself.

Problems in this process cause disorders and diseases.

The first author, Jacopo C. DiFrancesco, is qualified to discuss biology and neurology

because his credentials and experience include being a member of the Department of

Neurophysiology in Italy, being a member of the Department of Neurology at San Gerardo

Hospital, and publizing other scholarly articles like TREX1 C-terminal frameshift mutations in
the systemic variant of retinal vasculopathy with cerebral leukodystrophy. His contact

information is included in the article. The second author, Dario DiFrancesco, is qualified to

discuss biology and neurology because his credentials and experience include being a member of

the PaceLab, Department of Biosciences, and publizing other scholarly articles like Direct

activation of cardiac pacemaker channels by intracellular cyclic AMP. His contact information is

included in the article. The article was written 4 years ago. This source is current on the topic of

the sciences. The authors thoroughly evaluated all sides of the issue. For example, when

explaining hyperpolarization, the authors not only mentioned cellular excitability as a benefit of

hyperpolarization but also cellular generation and rhythmic activity. The coverage can be

considered broad because the author talks about hyperpolarization, depolarization, and

repolarization. The coverage can be considered deep because the author analyzes

hyperpolarization and all of its steps. The information contained in the source can be verified

elsewhere. For example, the author says HCN is open by hyperpolarization at resting membrane

voltage. This can be corroborated by the book by the name of Jasper’s Basic Mechanisms of

Epilepsy. In this publication, it is stated that HCNs are always open at resting potential with

hyperpolarization. The purpose of this article is to educate and inform the audience. The

audience is neurologists, biologists, and researchers. The article is appropriate for this purpose

and audience because it contains convoluted terms and ideas. For example, the article describes

hyperpolarization with the use of words like synaptic potentials and plasticity phenomena.
 Su, Z., Yang, Z., Xu, Y., & Yu, Q. (2015, February 21). Apoptosis, autophagy,

necroptosis, and cancer metastasis. Retrieved from https://molecular-

cancer.biomedcentral.com/articles/10.1186/s12943-015-0321-5

After most harmful mutation, apoptosis is triggered leading to the death of the cell with

the harmful mutation. Some cells with mutations get past apoptosis. These cells may lead to a

disease or disorder in later years. Apoptosis is programmed cell death. It occurs in old and

damaged cells. The process of apoptosis is as follows. Within the genetic material of each cell,

there is exonic DNA that results in the production of a protein that starts the process and signals

macrophages to approach the cell. When cells become old or damaged, they begin transcribing

and translating this piece of DNA. After this occurs, the cell starts getting smaller, and its

chromosomes begin condensing. Enzymes then start breaking down the cell and the cell wall.

After the enzymes have completed their processes, the cell starts spilling their contents in the

body of the organism. Some of the contents could possibly harm other cells, so macrophages

approach the contents of the destroyed cell and consume them. After this occurs, apoptosis has

been completed, and the cell has been removed. Several diseases like cancer work by bypassing

apoptosis. Cancer cells grow uncontrollably because there is no regulation on them by the body.

The first author, Zhenyi Su, is qualified to discuss biology and cells because

her credentials and experience include being a member of the Department of Biochemistry and

Molecular Biology at Southeast University and publicizing other scholarly articles like

MicroRNAs in apoptosis, autophagy and necroptosis. Her contact information is not included in

the article but can be found with further research. The second author, Zuozhang Yang, is

qualified to discuss biology and cells because his credentials and experience include being a
member of the Soft Tissue Tumors Research Center of the Yunnan Province and publicizing

other scholarly articles like Statins, autophagy and cancer metastasis. His contact information is

included in the article. This article was written 4 year ago. This source is current on the topic of

the sciences. The author thoroughly evaluated all sides of the issue. For example, when

describing programmed cell death, the authors do not only talk about apoptosis but also

autophagy and necroptosis. The coverage can be considered broad because the authors describes

all the steps and requirements for apoptosis. The coverage can also be considered deep because

they analyzed and explained the reasoning between each step of apoptosis. The information

contained in the source can be verified elsewhere. For example, the author says that dysfunctions

in cell death must be present for cancer metastasis to occur. This can be corroborated by an

article by the name of Metastasis: a question of life or death in his/her. In this publication, it is

stated that tumor metastasis possesses a resistance to apoptosis or cell death. The purpose of this

article is to inform and educate the audience. The audience is biologists and researchers. The

article is appropriate for this purpose and audience because it contains essential information and

complex terminology. For example, there are ideas such as cancer’s resistance to apoptosis, and

there are terms such as physical translocation.

 Saxena, P., Hamri, G. C.-E., Folcher, M., Zulewski, H., & Fussenegger, M. (2016,

February 2). Synthetic gene network restoring endogenous pituitary–thyroid feedback

control in experimental Graves' disease. Retrieved from

https://www.pnas.org/content/113/5/1244.short

There are many feedback loops within the body. If feedback loops are disrupted,

homeostasis is lost, and disease ensues. This is the case with Graves’ disease. There are two

types of feedback loops. The first type is positive feedback loops. In positive feedback loops,

when the stimulus results in the production of a hormone, the hormone increases the amount of

stimulus. As a result, this increases the production of the hormone. A good example of a positive

feedback loop is a population. As a population reproduces(stimulus), more offspring are created.

More offspring results in more future reproduction. The second type of feedback loop is negative

feedback loops. In negative feedback loops, when the stimulus results in the production of a

hormone, the hormone decreases the stimulus. This decreases the hormone produced. A good

example of a negative feedback loop is the relationship between insulin and blood glucose. As

blood glucose increases(stimulus), insulin is secreted. Insulin results in the intake of blood

glucose into the cells. This decreases the stimulus, the glucose in the blood. In Graves’ disease, a

negative feedback loop is disrupted. In the normal feedback loop, TRH from the hypothalamus

produces TSH which produces Thyroid hormones. Usually, the thyroid hormones decrease the

amount of TRH which ultimately decreases the amount of thyroid hormones. With Graves’

disease, however, the negative feedback loop is disrupted so thyroid hormones keep being

produced without being regulated.

 The first author, Pratik Saxena, is qualified to discuss biology, genetics, and feedback

loops because his credentials and experience include being a member of the Department of

Biosystems Science and Engineering in Switzerland and publicizing other scholarly articles like

Somatic embryogenesis and shoot regeneration from intact seedlings of Phaseolus acutifolius A.,

P. aureus (L.) Wilczek, P. coccineus L., and P. wrightii L. His contact information is not

included in the article but can be found with further research. The second author, Marc Folcher,

is qualified to discuss biology, genetics, and feedback loops because his credentials and

experience include being a member of the Department of Biosystems Science and Engineering in

Switzerland and publicizing other scholarly articles like Allosteric control of cyclic di-GMP

signaling. His contact information is not included in the article but can be found with further

research. This article was written 3 years ago. This source is current on the topic of the sciences.

The author thoroughly evaluated all sides of the issue. For example, when describing the current

solutions to Graves’ disease, the authors mention not only antithyroid drugs, their benefits, and

their drawbacks but also a closed loop gene circuit, their benefits, and their drawbacks. The

coverage can be considered broad because it describes both positive and negative feedback

loops. The coverage can be considered deep because it described each feedback loop in detail

with its relevance to Graves’ disease. The information contained in the source can be verified

elsewhere. For example, the author says Graves’ disease results in too much thyroid hormone

being produced. This can be corroborated by an article by the name of Graves' Disease. In this

publication, it is stated that a woman with Graves’ disease experienced extreme weight loss and

enlarging of the thyroid gland. These are common symptoms of too much thyroid hormone. The

purpose of this article is to inform and educate the audience. The audience is researchers and
biologists. The article is appropriate for this purpose and audience because it contains complex

ideas and terminology. For example, the article uses words like homeostasis and autoantibodies.

Y. Hovav, I. Kaminker, D. Shimon, A. Feintuch, D. Goldfarb, & S. Vega. (2014,

November 11). The electron depolarization during dynamic nuclear polarization:

measurements and simulations. Retrieved from

https://pubs.rsc.org/en/content/articlehtml/2015/cp/c4cp03825h.

Within a neuron, the resting voltage of the inner contents hovers around -70mV. Due to

external factors manifested from situations that arise around the body, voltage within the neuron

will increase. Not all external factors will, however, reach the required voltage to begin the

process of depolarization within the cell. This means that certain stimuli will not warrant a

response. When certain stimuli do, however, cause the neuron to increase in internal voltage to

-55 mV, the neuron will engage in depolarization. During depolarization, voltage increases due

to intakes of positively charged sodium ions. To offset this rapid gain in voltage, the neuron

releases positively charged potassium ions. Ultimately, this still leads to an increase in voltage

due to the decreased molecular weight of sodium ions which possesses a closer bond between the

protons and the electrons and a greater overall charge. The process of intaking and releasing

continues until receptors close off complex protein channels on the body of the neuron due to a

measure of the voltage of the inner body through proteins and substrates. On average, this

voltage is around 30 mV. This marks the end of depolarization with a greater concentration of

sodium ions in the body and a greater concentration of potassium ions in the environment.

Through the connection between repolarization and hyperpolarization, the devastating mechanics

of Alzheimer’s disease are demonstrated.

 The authors, Ilia Kaminker and Shimon Vega, are qualified to discuss depolarization and

the neuron’s communication network because their credentials and experience include being in

the Department of Chemical Physics at the Weizmann Institute of Science, working in the Tel

Aviv Institute on nuclear polarization, and publishing other scholarly articles such as

Simultaneous DNP enhancements of 1H and 13C nuclei: theory and experiments. Shimon

Vega’s contact information is included in the article. The article was written 5 years ago. This

source is current on the topic of the sciences. Even though this is an opinion, the authors still

present claims, reasoning, and evidence to show why that opinion is valid and credible. For

example, the authors talk about the incredible importance of depolarization within the cell in

communication to maintain homeostasis and supports that claim with facts about the mechanism

of depolarization. The coverage can be considered broad and deep because the authors discuss all

of the processes of depolarizations and its effects and causes, and the authors discuss how each

specific process contributes to the overall goal of raising the internal voltage. The information

contained in the source can be verified elsewhere. For example, the authors say depolarization

raises the voltage of the cell. This can be corroborated by Depolarization of Rat Brain

Synaptosomes Increases Phosphorylation of Voltage-sensitive Sodium Channels in which it is

stated that depolarization increases phosphorylation which results in increased voltage. The

purpose of this article is to educate the audience on depolarization. The audience consists of

researchers and neurologists. The article is appropriate for this purpose and audience because it

contains complex ideas, such as the thermal mixing mechanism and the DNP spectrum, and it

contains complex terms, such as double resonance.

 Barth, A. S., & Tomaselli, G. F. (2019, August 30). Repolarization Remodeling in

Structural Heart Disease. Retrieved from https://link.springer.com/chapter/10.1007/978-

3-030-22672-5_3.

After a neuron conducts depolarization due to a stimulus caused by external factors and

raises the voltage of the inner components of the cell to around +30 mV, the neuron will conduct

repolarization. The neuron can not stay at +30 mV with a sodium surplus for too long as the

excess sodium will start negatively reacting with the organelles of the neuron. During
repolarization, receptors on the body of the cell start instructing potassium protein channels to

open and intake potassium from the environment. While this is occuring, potassium sodium

pumps are moving sodium ions from the body of the cell to the environment through active and

facilitated diffusion. This process continues and leads to a decrease in the voltage of the cell.

Eventually, the receptors determine that the cell is at a low enough voltage, and through the use

of proteins and substrates, the receptors instruct the protein channels to close. The body now has

a great surplus of potassium ions, but it now possesses a voltage of -80 mV. This is too low, and

as a result, a process ensues. When considered with depolarization and hyperpolarization, the

malfunction of these processes can explain the mechanism of Alzheimer’s disease.

The authors, Andreas S. Barth and Gordon F. Tomaselli, are qualified to discuss

repolarization and action potentials because their credentials and experience include working in

the Albert Einstein College of Medicine in the Department of Medicine, working in the

Department of Cardiac Electrophysiology (Provides a neurology background), and publishing

other scholarly articles such as CAPON modulates cardiac repolarization via neuronal nitric

oxide synthase signaling in the heart. Both the authors’ contact information is included in the

article. This source was written several months ago. This source is current on the topic of the

sciences. Even though this is an opinion, the authors still present claims, reasoning, and evidence

to show why that opinion is valid and credible. For example, within the article, a central claim is

the prevalence of repolarization in communication between neurons and other bodily cells. The

authors then support this claim through scientific facts. The coverage can be considered broad

and deep because the authors discuss all the appliances of repolarization in communication and

how the disruption of any portion of the process negatively impacts the organism. The

information contained in the source can be verified elsewhere. For example, the authors say
repolarization lowers the voltage of the cell. This can be corroborated by Stepwise repolarization

from Ca2+ plateaus in neocortical pyramidal cells: evidence for nonhomogeneous distribution of

HVA Ca2+ channels in dendrites in which it is stated that repolarization does indeed lower the

voltage of the cell. The purpose of this article is to educate and inform the audience about

repolarization. The audience consists of researchers and neurologists. The article is appropriate

for this purpose and audience because it contains convoluted terms and ideas. For example, the

authors introduces ideas and terms such as heterogeneous changes and ionic current.

Lee, C.-H., & MacKinnon, R. (2017, January 12). Structures of the Human HCN1

Hyperpolarization-Activated Channel. Retrieved from

https://www.sciencedirect.com/science/article/pii/S0092867416317391.

After depolarization due to external stimuli causing a raise in voltage from approximately

-70mV to +30 mV and repolarization causing a decrease in voltage from approximately + 30 mV

to -80 mV, hyperpolarization begins to slightly increase the voltage back to the resting voltage of

-70 mV. This is completed as the neuron is most efficient in transferring signals at resting

voltage. During hyperpolarization, the receptors on the body of the neuron only activsyr the

potassium sodium protein channels to exchange 6 sodium ions for 4 potassium ions. This causes

a slight asymptotic increase to -70 mV as the neuron does not want to become too positive due to
efficiency. In the grand scheme of active potentials, hyperpolarization serves to delay action

potentials and repeated emission of neurotransmitters.

The authors, Chia-Hsueh Lee and Roderick MacKinnon, are qualified to discuss

hyperpolarization because their credentials and experience include working in the Department of

Structural Biology in the St. Jude’s Research Hospital, working in the Department of Molecular

Biology at Rockefeller University, and publishing other scholarly articles such as Pore loops: an

emerging theme in ion channel structure. Roderick MacKinnon’s contact information is included

in the article. The article was written 2 years ago and is current on the topic of the sciences. Even

though this is an opinion, the authors still present claims, reasoning, and evidence to show why

that opinion is valid and credible. For example, the authors discuss rhythmic circle’s importance

with hyperpolarization, and they support that by scientific fact based on their mechanism. The

coverage can be considered broad and deep because the authors cover everything relating to

hyperpolarization including rhythmic circles and surface proteins, but the authors still explain the

overall significance of each step and their role in maintaining homeostasis in communication.

The information contained in the source can be verified elsewhere. For example, the authors say

hyperpolarization raises the voltage inside of a cell slightly. This can be corroborated by

Hyperpolarized shifts in the voltage dependence of fast inactivation of Nav1.4 and Nav1.5 in a

rat model of critical illness myopathy in which it is stated that hyperpolarization increases the

voltage asymptotically. The purpose of this article is to educate and inform the audience. The

audience is researchers, biologists, and neurologists. The article is appropriate for this purpose

and audience because the article contains complex claims, including the significance of rhythmic

circles and circadians within communication and hyperpolarization, and complex terms, such as

nucleotide gated channels.

 Aurel, B. M., Arthur, K., Busche, M. A., Konnerth, A., Murphy, T., Marc Aurel Busche

Marc Aurel Busche Institute of Neuroscience, … Arthur Konnerth Institute of

Neuroscience. (2016, August 5). Impairments of neural circuit function in Alzheimer's

disease. Retrieved from

https://royalsocietypublishing.org/doi/full/10.1098/rstb.2015.0429.

Action potentials, within the neuron and axon, are combinations of processes of

depolarization, repolarization, and hyperpolarization. At the beginning of the long, thin, and rigid

portion of the axon in the neuron, localized depolarization begins with increases in the voltage of

the local area through influxes of sodium. After depolarization, the neuron engages in

repolarization and takes potassium from the environment and releases sodium. This continues

with hyperpolarization. Due to this sudden increase in sodium in the environment due to the

processes of the first localized area on the axon, the adjacent area begins the process of

depolarization while the first localized area finishes hyperpolarization. This pattern of localized
sodium surplus leading to adjacent depolarization continues down the axon until the last part of

the axon finishes hyperpolarization. By this time, the potential will have reached the dendrites of

the neuron. From these dendrites, the potential will continue through released neurotransmitters,

vacuole like substances that transfer information. These neurotransmitters meet the dendrites of

another neuron, and the signal continues into that neuron. After absorption of the

neurotransmitters, once again, the signal goes down the axon. This process continues and leads

to the transfer of information. A malfunction in this processes caused by a mechanism of

Alzheimer’s disease interrupts the transfer of information.

The authors, Marc Aurel Busche and Arthur Konnerth, are qualified to discuss action

potentials and their application because their credentials and experience include working in the

UK Dementia Institute, working in the Department of Neuroscience at the Technical University

of Munich, and publishing other scholarly articles such as Clusters of Hyperactive Neurons Near

Amyloid Plaques in a Mouse Model of Alzheimer's Disease. Both authors’ contact information

could be found with further research. The article was written 3 years ago and is current on the

topic of the sciences. Even though this is an opinion, the authors still presents claims, reasoning,

and evidence to show why that opinion is valid and credible. For example, the authors talk about

how Alzheimer’s primary cause is failure in the action potentials and supports that through

analyzing the symptoms of Alzheimer’s and the purpose of the action potential. The coverage

can be considered broad and deep because the authors talk about all of the components of the

Action potential, and the authors go into specifics about how each component creates and

contributes to the Action potential. The information contained in the source can be verified

elsewhere. For example, the authors say action potentials go down the axon of the neuron. This

can be corroborated by Membrane resting and action potentials from the squid giant axon in
which it is stated that action potentials do indeed go through the axon. The purpose of this article

is to educate and inform the audience. The audience consists of researchers and neurologists.

The article is appropriate for this purpose and audience because it contains intricate ideas of

neurology including oligomers, and it contains complex terminology including hyperactivity as

an example.

Weickenmeier, J., Jucker, M., Goriely, A., & Kuhl, E. (2018, October 15). A physics-

based model explains the prion-like features of neurodegeneration in Alzheimer's disease,

Parkinson's disease, and amyotrophic lateral sclerosis. Retrieved from

https://www.sciencedirect.com/science/article/pii/S0022509618307063.

Prions are specific versions of denatured proteins. Due to the way they unfold and come

apart upon denaturation due to an influx of temperature and pH, their amino acids rearrange in

such a way that they possess a highly dangerous ability of denaturing other proteins upon contact

with them. Prion presence creates immediate and great impacts to the homeostatic balance of the

body. Due to the importance of proteins ranging from surface channel proteins to reaction

catalyzing proteins (enzymes) within the body, prions can compromise the whole body. The

presence of prions marks the manifestation of neurological diseases such as Huntingson’s

disease. Due to the mechanism of prions, they act very similarly to Alzheimer’s disease. A

common treatment to prions is extended plasmid use, and as a result, it becomes logical that

plasmid use may be a logical treatment to Alzheimer’s disease.

 The authors, JohannesWeickenmeier and Mathias Jucker, are qualified to discuss prions

and genetics because their credentials and experience include working in the Department of

Cellular Neurology at the Hertie Institute, working in the Department of Mechanical Engineering

and Neurosciences at Stanford University, and publishing other scholarly articles such as Two

amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology.

Upon further research, both authors’ contact information can be found. The article was written

several months ago and is current on the topic of the sciences. The authors thoroughly evaluated

all sides of the issue. For example, they acknowledge how Alzheimer’s disease and Prions may

not be able to be compared due to the active denaturing of Proteins; however, The authors

address that opposing viewpoint by saying Alzheimer’s disease does destroy and denature

neurons and axons in the same way that Prions do with proteins. This inclusion shows that

alternative viewpoints to the authors’ were acknowledged because the authors mention an

opposing viewpoint but refutes it with logic. The coverage can be considered broad and deep

because the authors describe prions, their manifestation, their movement, and their development

but goes into detail about how each phase works, causes the next, and results in the development

of a deadly protein. The information contained in the source can be verified elsewhere. For

example, the authors says prion denature proteins. This can be corroborated by the article The

most infectious prion protein particles in which it is stated that Prions do denature proteins. The

purpose of this article is to inform and educate the audience. The audience consists of researchers

and neurologists. The article is appropriate for this purpose and audience because of the

convoluted themes, including denaturing and amino acid construction, and difficult terms, such

as amyloid deposits.

Ran, F. A., Hsu, P. D., Wright, J., Agarwala, V., Scott, D. A., & Zhang, F. (2013, October 24).
 Genome engineering using the CRISPR-Cas9 system. Retrieved from

https://www.nature.com/articles/nprot.2013.143

CRISPR, originating from bacterial origins, can be used by targeting a specific sequence

within the RNA. CRISPR is composed of bacterial plasmids and spaces, originating from

protospacers binding with associative PAM. The protospacers within each Cas9 are different

resulting in the different Cas9. Generally, there are two different types structures that aid Cas9.

The first is HDR. HDR, a mammalian repair system, produces cell lines that are to be used for

the double nicking of CRISPR. This allows specificality and the lack of error. The second is a

endonuclease. Programmable sequence specific endonuclease are really helpful for editing a

specific gene and aid CRISPR in specificality.

The author, Feng Zhang, is qualified to discuss genome editing because his credentials

and experience include membership of the Zhang lab, being in the department of Biological

Engineering, being in the institute of broad technology, and publishing a multitude of other

studies including Genome-Scale CRISPR-Cas9 Knockout Screening in Human Cells and

Rationally engineered Cas9 nucleases with improved specificity. His contact information is

included in the article. Written nearly 5 years ago, this source is current on the topic of the

sciences as the currency guideline for the sciences are 5 years. The author thoroughly evaluated

how all sides of the issue were acknowledged by the source. For example, the author describes

the many positives of the CRISPR system including the efficiency and specificality however, he

also discussed the limitations of the system including the PAM requirement present. The

coverage can be considered deep because the author goes in depth with the CRISPR technology

and its composition. The coverage can be considered broad because the author also describes the
many technologies that aid CRISPR in addition. The information contained in the source can be

verified elsewhere. For example, the author says CRISPR can be used by specifying a targeting

sequence within the RNA for efficient editing, which can be corroborated by Sophien Kamoun in

her publication Plant genome editing made easy: targeted mutagenesis in model and crop plants

using the CRISPR/Cas system in which she states CRISPR allows for specific editing through

non coding RNA. The purpose of this article is to inform and educate. The audience includes

experts of the field of genome editing. The article is appropriate for this purpose and audience

because of the high level vocabulary present. For example, words such as homology-directed

repair and endonucleases are used.

Landin-Romero, R., Kumfor, F., Leyton, C. E., Irish, M., Hodges, J. R., & Piguet, O.

(2016, March 21). Disease-specific patterns of cortical and subcortical degeneration in a

longitudinal study of Alzheimer's disease and behavioural-variant frontotemporal

dementia. Retrieved from

https://www.sciencedirect.com/science/article/abs/pii/S1053811916002378.
 For each patient and organism, at different stages, Alzheimer’s disease impacts different

levels of the neurological and physiological state of the brain at different times. That being said,

however, there have been developments that have isolated Alzheimer’s disease to specific areas

of the brain: the posterior cingulate area, the inferior parietal, and the striatum. These three areas

tend to experience the greatest impacts in atrophy and neuron lost. Through this establishment of

the location of typical Alzheimer’s disease, biomarkers can be used to guide medical treatments,

including drug use or plasmid use, towards these said certain areas in order to make them more

efficient.

The authors, Ramon Landin-Romero and Fiona Kumfor, are qualified to discuss

Alzheimer’s disease and the brain because their credentials and experience include working in

the Neuroscience Research Australia, working in the Australian Research Centre of Excellence

in Cognition, and publishing other scholarly articles such as Efficacy of Functional Remediation

in Bipolar Disorder: A Multicenter Randomized Controlled Study. Ramon Landin-Romero’s

contact information is included in the article. This article was written 3 years ago and is current

on the topic of the sciences. Even though this is an opinion, the authors still present claims,

reasoning, and evidence to show why that opinion is valid and credible. For example, the authors

state that Alzheimer’s disease is concentration in the posterior cingulate area, the inferior

parietal, and the striatum. The authors then support that through experiment data. The coverage

can be considered broad and deep because the authors describe all the areas in which degradation

are concentration, but the authors also go into depth into what the effects are of atrophy in each

specific area. The information contained in the source can be verified elsewhere. For example,

the authors say Alzheimer’s disease leads to degradation in the brain. This can be supported by

the article The significance of neuroinflammation in understanding Alzheimer’s disease which

states that Alzheimer’s disease leads to atrophy within the neurons in the cerebrum. The purpose

of this article is to inform the audience about a finding in a study. The audience consists of other

researchers and neurologists. The article is appropriate for this purpose and audience because it

contains complex ideas and themes such as atrophy in the cortical area and frontotemporal

dementia.

Raj, Divya, Yin, Marjolein, Janine, Holtman, … Inge R. (2017, June 12). Increased

White Matter Inflammation in Aging- and Alzheimer's Disease Brain. Retrieved from

https://www.frontiersin.org/articles/10.3389/fnmol.2017.00206/full.

Within the human brain, there is gray and white matter. The main neurons and cell bodies

reside within the gray matter, making the gray matter the more active portion of the brain.

Stimuli from external factors begin moving through the neurons in the gray matter portion of the

cerebrum. The white matter is where the isolated axons and dead neurons exist. The white matter
serves the purpose of transferring the information originating from the gray matter neurons to

other gray matter neurons. As of such, white matters exists between groups of gray matter

sections. During several neurological diseases, including Alzheimer’s disease, the white matter is

what is experiencing degeneration and atrophy. This means Alzheimer’s disease is not as much

as the killing of the neurons as it is the killing of the structures that move the information to the

neurons. This new development and understand will aid future treatments in specializing for

neurological disorders, including Alzheimer’s disease.

The authors, Divya Raj and Zhuoran Yin, are qualified to discuss gray and white matter

and neurology because their credentials and experience include working in the Department of

Neuroscience at the University of Groningen, working in the Department of Neurology at Tongji

Hospital, and publishing other scholarly articles such as An optimized protocol for the acute

isolation of human microglia from autopsy brain samples. Divya Raj’s contact information is

included in the article. The article was written 7 months ago and is current on the topic of the

sciences. Even though this is an opinion, the authors still present claims, reasoning, and evidence

to show why that opinion is valid and credible. For example, the authors talk about

neuroinflammation and its devastating nature on the mechanisms of the body due to Alzheimer’s

disease and supports the argument with facts and mechanisms. The coverage can be considered

broad and deep because the authors go over neuroinflammation on all parts of the brains and its

general impact on the whole body’s homeostatic balance, but the authors also go into specifics

about how it greatly impacts each area through neuron death and how it hurts each organ

systems. The information contained in the source can be verified elsewhere. For example, the

authors say white matter consists of axons. This can be corroborated by Regeneration of adult

axons in white matter tracts of the central nervous system which states that white matter does
consist of constantly regenerating axons. The purpose of this article is to inform and educate the

audience about Alzheimer’s disease’s impact on white matter. The audience is researchers and

neurologists. The article is appropriate for this purpose and audience because it contains highly

technical terms and systems such as neuroinflammation and oxidative stress.

Yu, Meichen, Engels, A., M. M., Hillebrand, Arjan, … J., C. (2017, March 16). Selective

impairment of hippocampus and posterior hub areas in Alzheimer's disease: an MEG-

based multiplex network study. Retrieved from

https://academic.oup.com/brain/article/140/5/1466/3072777.

With neurological disorders, especially Alzheimer’s disease, upon progression, decreased

activity can be seen within the command center of the body. Specifically, with Alzheimer’s

disease, the brain demonstrates a less defined C2 and C1 area and hippocampus in general, less

neuronal activity in the Middle Brain, cerebrum, Prefrontal cortex, and almost a complete lack

of neurons within the white matter portions of the brain. The lack of neuronal activity or neurons
provide a premonition to the effect of Alzheimer’s disease on the patient with each portion

generally be correlated to a certain action.

The authors, Meichen Yu and Marjolein M. A. Engels, are qualified to discuss the brain

and neurological disorders because their credentials and experience include working in the

Department of Clinical Neurophysiology in the Neuroscience Campus of Amsterdam and

publishing other scholarly articles such as Different functional connectivity and network

topology in behavioral variant of frontotemporal dementia and Alzheimer's disease: an EEG

study. Their contact information can be found upon further research. The article was written 2

years ago and is current on the topic of the sciences. The authors thoroughly evaluated all sides

of the issue. For example, they acknowledge that other regions of the brain do experience

atrophy, but they address that opposing viewpoint by discussing the relative low amount of

atrophy in other regions in typical cases of Alzheimer’s disease and supports that claim with

data. This inclusion shows that alternative viewpoints to the authors’ were acknowledged

because the authors state an opposing viewpoint and counters it. The coverage can be considered

broad and deep because the authors go through the many portions that are majorly impacted by

the degradation of neurological disorders, but also go into specific the current thinking into why

and how that influences the mechanism of Alzheimer’s disease. The information contained in the

source can be verified elsewhere. For example, the authors say that Alzheimer’s disease leads to

atrophy in neurons. This can be corroborated by the article Quantitative NMR measurements of

hippocampal atrophy in Alzheimer's disease in which it is stated that Alzheimer’s disease leads

to lower neuronal activity. The purpose of this article is to educate and inform the audience. The

audience is neurologists and researchers. The article is appropriate for this purpose and audience
because it develops its argument through complicated mechanisms such as connectivity

properties.

Cuyvers, E., & Sleegers, K. (2016, July). Genetic variations underlying Alzheimer's

disease ... Retrieved from https://www.thelancet.com/pdfs/journals/laneur/PIIS1474-

4422(16)00127-7.pdf.

As specific locations within the human genome in chromosomes 1, 19, 20, 5, X, and Y

have been identified as causing Alzheimer’s disease, the neurological disorder has been

identified as genetic in parts. Around 28%-30% of individuals who have contracted Alzheimer’s

disease have contracted it in part due to genetics. Siblings have a 50% chance of manifesting

Alzheimer’s disease in later parts of life if one or more of other siblings have contracted the

disease. The prevalence of genetically influenced manifestations of Alzheimer’s disease

continues to increase as Alzheimer’s disease continues to affect more and more people. As a

result, a genetic solution is becoming vastly more necessary. The plasmid solution would deal

with the genetic factors influencing contraction.

 The authors, Elise Cuyvers and Kristel Sleegers, are qualified to discuss genetics with

neurological diseases because their credentials and experience include working in the

Department of Molecular Genetics at the University of Antwerp, working in the Department of

Molecular Neurology at the University of Antwerp, and publishing other scholarly articles such

as Investigating the role of rare heterozygous TREM2 variants in Alzheimer's disease and

frontotemporal dementia. Kriestel Sleegers’ contact information is included in the article. The

article was written 3 years ago and is current on the topic of the sciences. The authors thoroughly

evaluated all sides of the issue. For example, the rebuttal to the authors’ argument stated that

their numbers were inaccurate as Alzheimer’s disease is also influenced by external factors. The

authors refuted that by stating that after so many trials with as many external factors made

constant as possible, the correlation between the genetics and manifestation of Alzheimer’s

disease must still be present. This inclusion shows that alternative viewpoints to the authors’

were acknowledged because the authors’ address the opposite view point and states how it makes

no difference in what they are trying to communicate. The coverage can be considered broad and

deep as the authors’ go over all of the genetic factors influencing manifestation of the disease

and goes into detail about the specific factors. The information contained in the source can be

verified elsewhere. For example, the authors say that Alzheimer's disease is influenced by

genetic factors, which can be corroborated by Molecular genetics of Alzheimer's disease and

aging which states that Alzheimer’s disease has been shown to be caused by genetic factors. The

purpose of this article is to inform the audience. The audience consists of researchers and

neurologists. The article is appropriate for this purpose and audience because the authors use

complex ideas such as intragenic copies to make their point.

 Wu, Y., Zhou, H., Fan, X., Zhang, Y., Zhang, M., Wang, Y., … Li, J. (2014, December

5). Correction of a genetic disease by CRISPR-Cas9-mediated gene editing in mouse

spermatogonial stem cells. Retrieved from https://www.nature.com/articles/cr2014160.

Plasmids have been used with another genetic disease and have produced favorable

results. During an experiment, certain mice were genetically altered to develop and exhibit a

genetic disease. Researchers, after determining the mice did indeed contract said genetic disease,

used the CRISPR Cas9 genome editing tool to insert plasmids in precise locations on the

genome. The plasmid, containing recombinant DNA, replaced the genes that produced proteins

that exhibited that genetic disease. After administration, 70%-80% no longer exhibited the

disease. With promising results in administration to said mice with the genetic disease, the same

promising results should be yielded when tested with Alzheimer’s disease.

The authors, Yuxuan Wu and Jinsong Li, are qualified to discuss plasmid use and

genetics because their credentials and experience include working in the Shanghai Key

Laboratory of Molecular Andrology at the Institute of Biochemistry and publishing other

scholarly articles such as Directly transforming PCR-amplified DNA fragments into plant cells is

a versatile system that facilitates the transient expression assay. Jinsong Li’s contact information
is included in the article. The article was written 5 years ago and is current on the topic of the

sciences. Even though this article is opinionated, the authors’ still presents claims, reasoning, and

evidence to show why that opinion is valid and credible. For example, the authors state that

plasmids will be an effective tool for solving genetic problems and supports this from data from

their experiment. The coverage can be considered broad because the authors go over stem cells,

plasmids, and the genome. The coverage can be considered deep because the authors go over the

details of how each specifically affects the experiment. The information contained in the source

can be verified elsewhere. For example, the authors state that plasmids can be used for gene

therapy. This can be corroborated by Gene Therapy by Intramuscular Injection of Plasmid DNA:

Studies on Firefly Luciferase Gene Expression in Mice in which it is stated that plasmid injects

cause reorganization of the genome through gene therapy. The purpose of this article is to inform

the audience about a claim and support it through evidence. The audience is researchers,

neurologists, and geneticists. The article is appropriate for this purpose and audience because it

contains complex themes, including Spermatogonial stem cell alteration, to support its main

claim.

Cass, S. P. (2017). Alzheimer's Disease and Exercise: A Literature Review : Current Sports

Medicine Reports. Retrieved November 1, 2019, from https://journals.lww.com/acsm-

csmr/FullText/2017/01000/Alzheimer_s_Disease_and_Exercise___A_Literature.9.aspx.

The prevalence of Alzheimer’s disease, a neurological disorder, has been correlated with

external factors such as a lack of constant mental exercise, including the absence of mentally

stimulating actions such as puzzles or learning new information; a lack of physical exercise,

including the absence of cardiovascularly stimulating actions such as jogging; and a poor diet,

including low consumption of varied vitamins. Specifically, through the evaluation of an

experimental data collection in which mice with early symptoms of Alzheimer’s disease were

provided with differing levels of cardiovascular movement, exercise has been correlated with

several increases in homeostatic expression in the body. Firstly, exercise has been shown to

increase blood flow to the brain organ and brain cells. This leads to increased stimulation of the

neurons, resulting in increased signal transmission which decreases the chance of the

manifestation or spread of Alzheimer’s disease within the neuron due to decreased amyloid

buildup. Secondly, exercise has been correlated with increased size of the hippocampus, C1, and

C2 area due to increased neuron production, decreasing the amyloid buildup and preventing

Alzheimer’s disease. Finally, exercise has been demonstrated to stimulate neurogenesis, the

creation of neurons, through increased oxygen intake as a result of increased blood flow to the

brain. This, once again, prevents amyloid build up and prevents the spread of Alzheimer’s

disease. As a result, external factors, especially physical exercise, are possible treatments to

Alzheimer’s disease.

The author, Shane Cass, is qualified to discuss the relationship between cardiovascular

exercise and Alzheimer’s disease because his credentials and experience include being a doctor

of Sports Medicine located at the University of New Mexico and publishing other scholarly

articles based on Dementia such as Cognitive assessment in a predominantly Hispanic and

Native American population in New Mexico and its association with kidney transplant wait‐

listing. His contact information is included in the article. The article was written 2 years ago,

which is current on the topic of the sciences and medicine. Even though this article is an

opinionated creation, the author still presents claims, reasoning, and evidence to show

why that opinion is valid and credible. For example, the author claims that exercise is a possible

treatment for Alzheimer’s disease. He then supports this by explaining how exercise contributes
to increased hippocampus size, for example, which ultimately decreases amyloid count and

Alzheimer’s disease. The coverage can be considered broad because the author lists the many

reasons why exercise contributes to decreases in Alzheimer’s disease. The coverage can be

considered deep because the author goes in depth when explaining each reason why exercise

contributes to decreased contraction by explaining the mechanisms and how that connects to

decreased amyloid production. The information contained in the source can be verified

elsewhere. For example, the author says Alzheimer’s disease leads to worse memory, which can

be corroborated by Alzheimer's Disease Is a Synaptic Failure. In this publication, it is stated that

Alzheimer’s disease leads to a deterioration in memory. The purpose of this article is to educate

and inform the audience in order to increase knowledge of the disease. The audience

is researchers, geneticists, and pathologists. The article is appropriate for this purpose and

audience because of the complex ideas and sophisticated vocabulary introduced. For example,

The article uses terminology such as neurogenesis and hippocampal volumes and presents ideas

such as improved neurogenesis through more active neurons and increased blood flow leading to

decreased amyloid build up.