UNIVERSIDAD NACIONAL MAYOR DE SAN MARCOS

(Universidad del Perú, DECANA DE AMÉRICA)

FACULTAD DE MEDICINA
ESTUDIOS GENERALES

MONOGRAPH ON THE PATHOLOGY OF ALZHEIMER'S

MEMBERS:

● Blas Melgarejo Marco Andrés Aarón

● Chumpitaz Garcia Yamile Shirley
● Luna Mendoza Jean Carlos
● Rodríguez Campos Flavia Alexia
● Rojas Tafur Jesus Valentin
● Villegas Robles Roger Alberto

TEACHER:

BRAYAN KEVIN LAGUNA CHAVEZ

COURSE

Inglés Aplicado a Ciencias de la Salud II

GROUP 3

LIMA - PERÚ
2022
 Dedication

We dedicate this work to God and our parents for the desire to improve and
love that they give us every day in which they have been able to guide our lives
along the path of wisdom and truth, giving us the future of their effort and
sacrifice for offering us a better tomorrow. Also, we dedicate our work to the
professor of the course, for teaching us everything we know and guiding us to
be a better person and professional.
INDEX

Contenido
1. ORIGIN-HISTORY.............................................................................................................. 5
2. DESCRIPTION ................................................................................................................... 6
3. Types.................................................................................................................................. 7
3.1. Familial or sporadic: ........................................................................................................ 7
3.2 Age of appearance: .......................................................................................................... 7
4. SYMPTOMS ....................................................................................................................... 8
5. DIAGNOSIS AND TREATMENT ....................................................................................... 8
5.1 Central diagnostic criteria: ............................................................................................... 9
5.2 Features that support the diagnosis: ............................................................................... 9
6. MEDICATIONS................................................................................................................. 11
7. CONCLUSIONS ............................................................................................................... 12
8. BIBLIOGRAPHIC REFERENCES ................................................................................... 13
9. ANNEXES ........................................................................................................................ 14
 1. ORIGIN-HISTORY

It has been more than a century since this disease was discovered and scientists have
worked to discover how it works and the causes that generate it, as well as to find the
drugs that can stop it.

● 1906, the German doctor and scientist Alois Alzheimer presented the case of
Mrs. Auguste Deter, a 50-year-old patient whose husband had taken her to the
hospital after detecting changes in her behavior. Those first symptoms would
later be recognized as the disease that would bear his name. The patient
experienced memory loss, paranoia, and psychological changes. Dr. Alzheimer
noted at autopsy that there was shrinkage in and around the nerve cells in his
brain.
● In 1910 Kraepelin named the disease Alzheimer's in recognition of Dr. Alois's
discovery of the disease.
● In 1968: Cognitive measurement scales are created that allow researchers to
measure deterioration and estimate the volume of damaged brain tissue.
● In 1974: Congress established the National Institute on Aging (NIA).
● In 1983, the first National Alzheimer's Disease Month was declared, signaling
increased awareness of the disease.
● In 1984: The NIA began funding the Alzheimer's Disease Centers and
established a national network for Alzheimer's disease research.
● In 1993: The Food and Drug Administration (FDA) approved the first
Alzheimer's drug, Cognex. The drug targets memory loss and dementia
symptoms.
● In 2003: The NIA began a national genetic study of Alzheimer's disease to
identify risk genes for the disease.
● In 2010, the preclinical phase in Alzheimer's disease was defined, a silent stage
of long duration, which precedes the manifestation of symptoms by 15 or 20
years
● In 2013: The G8 Dementia Summit in the UK launched an international effort to
fight the disease and find a cure by 2025.
● In 2014. In the United States they designed the first clinical trial for the
prevention
● In 2015, the EPAD Consortium was born, one of the most important initiatives
in the world for research into Alzheimer's prevention
 2. DESCRIPTION
Microscopic changes in the brain begin long before the first signs of memory loss. The
brain has 100 billion nerve cells (neurons). Each nerve cell connects with many others
to form communication networks. Groups of nerve cells have special jobs. Some are
involved in thinking, learning, and remembering. Others help us see, hear and smell.

To do their work, brain cells operate like tiny factories. They receive supplies, generate
energy, construct equipment, and get rid of waste. Cells also process and store
information and communicate with other cells. Keeping everything running requires
coordination as well as large amounts of fuel and oxygen.

Scientists believe Alzheimer's disease prevents parts of a cell's factory from running
well. They are not sure where the trouble starts. But just like a real factory, backups
and breakdowns in one system cause problems in other areas. As damage spreads,
cells lose their ability to do their jobs and eventually die, causing irreversible changes
in the brain.

People with Alzheimer’s have trouble doing everyday things like driving a car, cooking
a meal, or paying bills. They may ask the same questions over and over, get lost easily,
lose things, or put them in odd places, and find even simple things confusing. As the
disease progresses, some people become worried, angry, or violent.

The time from diagnosis to death varies as little as three or four years if the person is
older than 80 when diagnosed, to as long as 10 or more years if the person is younger.

Currently, there is no cure for Alzheimer’s disease, though there has been significant
progress in recent years in developing and testing new treatments.
 3. TYPES

3.1. Familial or sporadic:

Depending on its cause, at least as far as the causes of Alzheimer's are currently
known, we can talk about:

Familial Alzheimer's: These are rare cases, but they do happen. Certain genetic
mutations can be in a family and be inherited from generation to generation. The
“familial” variant represents only less than 1% of Alzheimer's cases. In them, the
disease usually has a very early onset, and the symptoms frequently appear before
the age of 60 and may even manifest themselves in the 40s. It should be noted,
however, that not all cases of early onset (below 60 years of age) are genetically
determined, but sporadic (i.e., not genetically determined) Alzheimer's disease can
also occasionally appear in this age range. age. The family pattern is basically
characterized by at least three cases in two or more consecutive generations, and all
diagnosed before the age of 60.

Sporadic Alzheimer's: in most patients the cause of the disease is unknown, hence it
is called sporadic Alzheimer's.

3.2 Age of appearance:

Depending on the age at which the patient begins to show symptoms, we can talk
about:

Early-onset Alzheimer's: generally, corresponds to the cases that we mentioned

before, to people who have familial Alzheimer's. In them the disease appears before
the age of 65, even before the age of 40, but its evolution and symptoms are like those
of people with sporadic Alzheimer's.

Late-onset Alzheimer's: When the disease becomes evident after the age of 65 (some
researchers prefer to put that limit at 60 years), it is called late-onset Alzheimer's. It is
the most common form of the disease, of which its causes are not known so far.
 4. SYMPTOMS

Today, we know that the brain changes typical of Alzheimer's disease begin years
before the first symptoms appear.

The symptoms of this disease are of two types:

On the one hand, those related to the loss of brain functions of a cognitive nature that
allow us to relate to the environment and to other people: loss of memory, language,
attention and orientation.
And on the other, the alteration of emotional and behavioral skills: with changes in
motivation, mood, character and even sleep.
This symptomatology manifests itself progressively and gradually, in stages, and
depending on the phase in which the patient is, the symptoms are different and severe.
In total, it is estimated that the evolution of symptoms spans between 5 and 15 years.

Finally, the most common symptoms are:

● Cognitive impairment. (SEE THE FIGURE 1 IN ANNEXES)

● Temporo-spatial disorientation. (SEE THE FIGURE 2 IN ANNEXES)
● Difficulty expressing yourself.
● Difficulty performing activities of daily living.

5. DIAGNOSIS AND TREATMENT

Due to the need for treatments for Alzheimer's disease in its initial phases, its early
detection has become one of the research foci in the field of neurodegenerative
diseases.

Currently, the diagnosis of Alzheimer's disease is based on the clinic, since biological
markers have been established with necessary reliability and specificity. General
criteria for dementia and other specific ones have been defined

These criteria mention us that, to establish the definitive diagnosis of Alzheimer's

disease, histopathological confirmation is necessary, while the diagnosis of probable
EA can be done if there is an insidious and progressive start dementia in the absence
of other systemic or cerebral diseases that they can explain cognitive disorder.
 5.1 Central diagnostic criteria:

Presence of significant episodic memory alteration that includes the following

characteristics: gradual and progressive change of the music function referred to by
patients of at least six months of evolution, objective evidence of the significant
alteration of the episodic memory measured by test and that the alteration of episodic
memory can be associated with other cognitive changes. (Valls-Pedret tape, José Luis
Molinuevo, Lorena Rami, 2010) (SEE THE FIGURE 2 IN ANNEXES)

5.2 Features that support the diagnosis:

Presence of atrophy of the medial temporal lobe: loss of hypocampal volume,

entorrinal cortex and tonsil, evidenced by visual qualitative changes observed in
magnetic resonance (taking into account the characteristics of the population of the
same age) or quantitative changes evaluated by studies of studies of volumetry in the
regions of interest (taking into account the norms of the population of the same age).

Abnormal biomarker in cerebrospinal fluid: low beta-amyloid concentrations, high

concentrations of tau or increased concentrations of phospho-tau or combination of
these three.

Specific brain functional pattern by positron emission tomography: reduction of

metabolism in temporarietal areas.

Autosomic dominant mutation proven with a first -degree relative affection.

Exclusion criteria

History: acute home; Early appearance of the following symptoms: alteration of the
march, epileptic crises, behavioral changes.

Clinical features: focal neurological signs, including hemiparesis, sensitive loss, deficit
in visual fields and early extrapyramidal signs.

Other disorders that cause memory alteration or related symptoms:

- No EA type dementia

- Major depression

- Cerebrovascular disease
- Toxic and metabolic alterations, which will require a specific study

- Abnormalities detected in Magnetic resonance sequences Flair or T2 in the medial

lobe compatible with infectious or vascular processes.

Definitive criteria for Alzheimer's disease: It is definitive if the following criteria are
present: clinical and histopathological evidence of the disease (through cerebral
autopsy or biopsy) and evidence of clinical and genetic criteria of Alzheimer's disease
(mutations in the chromosome 1, 14 or 21); Both criteria must be present.

Currently, treatment for Alzheimer’s disease does not impact the progression or
underlying pathology of the disease. However, with medication and other therapies,
steps are taken to increase the quality of life of those with Alzheimer Disease. Current
therapeutics are based off the Cholinergic Theory, which attributes a decrease in
cholinergic neurotransmission to a decline in cognitive function. At present, there are
two classes of pharmacologic therapy available for Alzheimer Disease: cholinesterase
inhibitors (donepezil, rivastigmine, and galantamine) and memantine, which has
activity as both a non-competitive N-methyl-D-aspartate receptor antagonist and a
dopamine agonist . The cholinesterase inhibitors are approved for use in patients with
mild, moderate, or severe AD dementia as well as Parkinson’s disease dementia.
Memantine is approved for use in patients with moderate to severe Alzheimer Disease
who may also have difficulty with alertness and attention.

Other aims of treatment look to modifiable risk factors in one’s overall health and
“cognitive reserve” including cardiovascular/lifestyle factors, such as a healthy diet and
plenty of physical exercise, as well as cognitive engagement. Cognitive reserve refers
to the ability to fend off pathologic insult, meaning the ability to engage alternate
synaptic pathways or cognitive strategies to cope with the pathology of Alzheimer
Diseases
 6. MEDICATIONS

Treating the symptoms of Alzheimer's disease can provide comfort, dignity and
independence to people with Alzheimer's disease for a longer period of time, and can
also encourage and help their caregivers. Galantamine, rivastigmine and donepezil,
which are cholinesterase inhibitors, are prescribed for mild to moderate symptoms of
Alzheimer's disease. These medications may help reduce or control some cognitive
and behavioral symptoms

Medications for moderate to severe Alzheimer's disease

Aricept® is also approved to treat moderate to severe Alzheimer's disease. Another
drug, Namenda®, can decrease symptoms, which may allow some people to do more
things for themselves, such as use the toilet. The generic name for this drug is
memantine.

Sometimes doctors use more than one drug to treat moderate to severe Alzheimer's
disease. For example, they might use Aricept® and Namenda®, which work in
different ways. Another drug, Namzaric®, combines donepezil and memantine in a
single pill.(SEE THE FIGURE 4 IN ANNEXES)
7. CONCLUSIONS

● Alzheimer's disease could become a serious public health problem in the

coming decades, generating a state of dependency with a high psychological,
moral, social and economic cost, making early diagnosis necessary. Many
people have trouble with memory but this does not mean they have Alzheimer's.
There are many different causes of memory loss. If you or someone you know
is experiencing symptoms of dementia, it is best to visit a doctor so the cause
can be determined.
● Alzheimer's disease is a progressive brain disorder, in which the brain gradually
degenerates. It occurs most often in people over 65 or 70 years of age.
Throughout the disease, parts of the brain degenerate, leading to cell loss and
dysfunction, gradual loss of memory, impaired reasoning or judgment,
disorientation, learning difficulties, loss of language ability, and decreased
ability to perform routine tasks
● The cause of Alzheimer's disease remains unknown. There is still no treatment
that can reverse or slow the progression of the disease. Large-scale population
studies have revealed that individuals who follow a healthy diet and adopt a
positive lifestyle have a much lower risk of Alzheimer's disease than populations
who smoke, eat an unhealthy diet and do not exercise. Walking, exercising, and
losing weight would help us not only to suffer from the risk of this disease, but
also greatly nourishes the brain and body, and improves the quality of life.
● To prevent Alzheimer's, a balanced diet should be followed, such as the
Mediterranean diet, which includes plenty of vegetables, fruits and lean protein,
especially protein sources that contain omega fatty acids. Be physically active
and be socially active, which includes aerobic exercise.
8. BIBLIOGRAPHIC REFERENCES

● Alzheimer [Internet]. Cinfasalud. [citado 8 de noviembre de 2022]. Disponible

en: https://cinfasalud.cinfa.com/p/alzheimer/
● Enfermedad de Alzheimer: Síntomas, diagnóstico y tratamiento. CUN
[Internet]. [citado 8 de noviembre de 2022]. Disponible en:
https://www.cun.es/enfermedades-tratamientos/enfermedades/enfermedad-
alzheimer
● ¿Existen varios tipos de Alzheimer? [Internet]. TiTi. 2017 [citado el 9 de
noviembre de 2022]. Disponible en: https://infotiti.com/2017/03/existen-varios-
tipos-alzheimer/
● Fundalzheimer.com. [citado 9 de noviembre de 2022]. Disponible en:
http://fundalzheimer.com/wp-content/uploads/2019/01/AC-Diagnostico-
precoz-de-la-enfermedad-de-Alzheimer.pdf
● Mcgirr S, Venegas # C, Swaminathan A. Alzheimer’s Disease: A Brief Review
[Internet]. Scientificarchives.com. [citado 9 de noviembre de 2022]. Disponible
en: https://www.scientificarchives.com/admin/assets/articles/pdf/alzheimers-
disease-a-brief-review-20200729110737.pdf
● Maragall FP. Historia del Alzheimer: cronología de la enfermedad y su
investigación [Internet]. Fpmaragall.org. [citado el 9 de noviembre de 2022].
Disponible en: https://blog.fpmaragall.org/historia-del-alzheimer
● Yang HD, Kim DH, Lee SB, Young LD. History of Alzheimer’s disease. Dement
Neurocognitive Disord [Internet]. 2016 [citado el 9 de noviembre de
2022];15(4):115–21. Disponible en:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6428020/
● Sauer A. History of Alzheimer’s: Major milestones [Internet]. Alzheimers.net.
2013 [citado el 9 de noviembre de 2022]. Disponible en:
https://www.alzheimers.net/history-of-alzheimers
● Maragall FP. Alzheimer “familiar”: cuando la genética es determinante
[Internet]. Fpmaragall.org. [citado el 9 de noviembre de 2022]. Disponible en:
https://blog.fpmaragall.org/alzheimer-familiar
 9. ANNEXES

1. 2.

3.
4.