Assessment Task-3 (Dementia Disease)

1. Multi Infarct Disease:

Description: 'Multi-infarct' means that due to a loss of oxygen from a number of minor strokes, several
parts of the brain have been damaged. Blockages in the brain vessels typically cause a stroke
(infarction), but there are no signs of a stroke often. These "silent" strokes raise the risk of vascular
dementia in an individual.

Symptoms: The symptoms of Multi-infarct disease are:

 Confusion and restlessness.

 Problems in recollection or thought problems.
 Tingling or numbness.
 Frequency or incontinence in urine.
 Attention, concentration and judgment difficulties.
 An lack of feeling.
 Withdrawal from contact with culture.
 Planning difficulties ahead.

Usual age range of onset: Multi-infarct dementia typically affects persons between 60 and 75 years of
age. Men are slightly more likely to have this illness than females. However, elevated blood pressure
remains the most significant risk factor for multi-infarct dementia. Developing multi-infarct dementia is
rare for a person without elevated blood pressure.

Changes that Occur in Brain: A general cause of memory loss in the elderly is multi-infarct dementia
(MID). MID is activated by different strokes (disruption of blood flow to the brain). Blood supply
disturbance contributes to weakened brain tissue. Without visible health signs, some of these strokes
can occur.

How the disease typically progresses: The most prevalent cause of vascular dementia is potentially this.
A variety of strokes cause multi-infarct dementia, often with signs that grow gradually over a period of
time. The strokes cause damage to the brain cortex, the learning-related region, memory and language.
In the early stages, an individual with multiinfarct dementia is expected to have greater intuition than
individuals with Alzheimer's disease, and aspects of their personality can remain relatively intact for
longer. Extreme depression, mood swings and seizures can be signs. Since multi-infarct dementia
symptoms may evolve in stages, it is easy to confuse them with Alzheimer's disease. However, types of
vascular dementia frequently occur with Alzheimer's, and some literature indicates that multi-infarct
dementia can worsen or contribute to the development of Alzheimer's disease.

What current research is being done? : A variety of Alzheimer's Society sponsored projects concentrate
on whether care for blood and cardiac disorders could reduce the risk of vascular dementia. Dr Atticus
Hainsworth at St George's University, London, is running one programme. In order to see if an existing
drug called tadalafil can increase blood flow to areas of the brain that are vulnerable to the condition, Dr
Hainsworth is conducting a drug trial. This increased flow of blood can help reduce brain cell damage
and decrease the risk of developing vascular dementia. Tadalafil acts by blocking an enzyme known as
PDE5, and tadalafil is currently used in a similar manner to Viagra! This method also has other
applications! Professor Allison Halliday and her colleagues at Oxford University are tackling the topic
from a new perspective. They are studying whether people who have undergone surgery to reduce the
likelihood of a stroke are now less likely to develop vascular dementia. Widening the carotid artery,
which supplies the brain with blood, was involved in this procedure.

2. Huntington’s disease:
Description: Huntington's disease is a gradual brain disorder that induces spontaneous gestures, mental
problems and lack of capacity to think (cognition). The most prevalent type of this condition, adult-onset
Huntington disease, typically occurs in the thirties or forties of a person. A chronic brain dysfunction
caused by a single mutated gene on chromosome 4, one of the 23 human chromosomes bearing the
entire genetic code of an individual, is Huntington's disease. This defect is "dominant," meaning that the
condition will inevitably evolve through someone who inherits it from a parent with Huntington's.

Symptoms: Irritability, depression, slight repetitive gestures, impaired balance, and difficulty processing
new knowledge or making choices may be early signs and symptoms. Many persons with Huntington's
disease develop gestures of repetitive jerking or twitching known as chorea. These movements are
getting more pronounced as the disease advances. Affected patients may have difficulties walking,
listening, and swallowing. People with this condition also undergo personality changes and a
deterioration in skills in thought and reasoning. After signs and symptoms begin, persons with the adult-
onset form of Huntington disease typically live between 15 to 20 years.

Usual age range of onset: Huntington's disease signs typically manifest between the ages of 30 and 50,
but can begin as early as 2 years of age or as late as 80. Uncontrolled movement of the arms, legs, back,
face and upper body is the signature characteristic of Huntington's disease.

Changes that Occur in Brain: Sections of the brain that help smooth and organize gestures degenerate
during Huntington disease. Movements are jerky and uncoordinated, and mental capacities are
weakening, including self-control and memory. Doctors base the diagnosis on symptoms, history of the
family, brain scans, and genetic tests. Drugs can help ease the symptoms, but the disease is incremental,
gradually resulting in death. Huntington's disease is caused by the progressive degeneration of the
caudate nucleus and putamen, members of the basal ganglia. Basal ganglia is a group of nerve cells
found deep within the brain at the base of the cerebrum. They help smooth out gestures and organize
them.

How the disease typically progresses: The cognitive abilities of an individual steadily degrade over time
after Huntington's disease begins. The rate of development and length of diseases vary. The duration
from the onset of sickness to death is often around 10 to 30 years. After signs arise, juvenile
Huntington's disease typically results in death within 10 years. Huntington's disease-related psychiatric
depression can raise the risk of suicide. Any evidence shows that the higher likelihood of suicide comes
before a diagnosis is made and when a person tends to lose independence in the middle stages of the
illness. He or she is likely to be confined to a bed late in the illness and unable to speak. Someone with
Huntington's disease is normally capable of recognizing language and is mindful of family and friends,
but others may not know members of the family.

What current research is being done? : Major researches being done in HD are:

 Basic neurology: Now that the HD gene has been identified, researchers are studying the
nervous system's anatomy, physiology, and biochemistry to define how it causes illness in the
human body.
 Clinical Research: While seeking to find alternative approaches, neurologists, physicians,
clinicians, and other experts are developing our understanding of medical signs and disease
development.
 Imaging: Science analysis using specialized technology helps scientists to imagine what the faulty
gene is doing to the brain's mechanisms and chemicals.
 Animal Models: HD is studied via laboratory animals.
 Fetal Tissue Research: In order to recognize and correct nerve cell degeneration, scientists are
implanting fetal tissue in mice and nonhuman primates.

3. Pick’s Disease
Description: Pick's disease is a rare form of age-related dementia that attacks the brain's frontal lobes
and induces trouble with speech such as aphasia, difficulty with actions and ultimately death. It was first
identified in 1892 by Arnold Pick, a Czech neurologist and psychiatrist. Pick's disease is used
interchangeably for "frontotemporal dementia" in several older psychiatric texts, but Pick's disease is
known to be one of three very particular forms of frontotemporal dementia in clinical medicine. Your
brain uses a distribution mechanism to help the nutrients it requires pass through. This system is made
of proteins that direct nutrients where they need to go, like railroad tracks to guide trains. They are also
tau proteins, the proteins that hold the tracks straight. When you have Pick's disease, the tau proteins
don't function the way they should. You may have more of them in your brain than most individuals,
too. They are called Pick bodies, these irregular clumps of tau proteins. Select bodies that "derail" the
transport system. The track is no longer straight, because there is no way for nutrients in the brain to go
where they have to go. This does damage to the brain that can not be reversed.

Symptoms: It may be tough for doctors to distinguish between forms of dementia. Alzheimer's disease,
the most prominent form of dementia, can also be distinguished from frontal lobe dementia like Pick's
disease because memory loss is one of the first notable signs of Alzheimer's. Frontal lobe dementia, in
its early stages, is not usually associated with memory loss. Particularly for the aphasia it causes, Pick's
disease is recognised. This will differentiate it from other forms of frontotemporal dementia, in which
behavior disturbances and personality changes are also a primary first symptom. That said, behaviour
issues can also be associated with Pick's disease. It is not always possible to decide with certainty
whether a patient has Pick's disease, some form of frontal lobe dementia, or an entirely different cause
of aphasia.

Usual age range of onset: In individuals as young as 20, it can occur. But it generally starts between the
ages of 40 and 60. The average age that it starts at is 54.

Changes that Occur in Brain: Pick's disease is caused by abnormal amounts or kinds of nerve cell
proteins, called tau, along with other FTDs. In all of your nerve cells, these proteins are found. They
often accumulate into spherical clumps, known as Pick bodies or Pick cells, if you have Pick's disease.
When they accumulate in the frontal and temporal lobe nerve cells of your brain, they cause the cells to
die.

How the disease typically progresses: Although some cases progress slowly, Pick's disease typically
proceeds quicker than AD, taking just four or six years on average from diagnosis to death. Patients with
improvements in behaviour appear to take a more accelerated path. Pick's illness is triggered in the
brain by an accumulation of tau proteins, dubbed "Pick bodies." Pick bodies cause brain trauma that
affects (but is not limited to) the frontal lobes in areas where they are present. In the brains of
Alzheimer's patients, Tau proteins still build up, but only one source of these tau proteins is
predominant in the brains of people with Pick's disease. This distinction helps researchers and
pathologists to distinguish Pick's disease from Alzheimer's disease postmortem.

What current research is being done? : Pick's disease, primary progressive aphasia, and semantic
dementia are combined as FTD in the new classification of the condition classes. Many doctors
recommend that FTD be applied to corticobasal degeneration and progressive supranuclear palsy and
name the group Pick Complex. There will continue to be controversy about these designations. The
symptoms of FTD fall into two clinical trends, as described today, that include either (1) changes in
behaviour or (2) language problems. The first category includes actions that may be either impulsive
(disinhibited) or bored and listless (apathetic) and contains unwanted social behavior; loss of social
touch; lack of empathy; distractability; heightened interest in sex; changes in food preferences; or, on
the other hand, blunted emotions; avoidance of personal hygiene; excessive or compulsive behavior;
and reduced energy and enthusiasm. The second type mostly features language disruption symptoms,
including difficulties making or interpreting speech, mostly in conjunction with the symptoms of the
behavioral type. Spatial ability and memories stay intact. The disorder has an important genetic
component; FTD also runs in families.
 4. Dementia with Lewy Bodies:
Description: The disorder associated with excessive deposits of a protein called alpha-synuclein in the
brain is Lewy body dementia (LBD). These deposits, called Lewy bodies, affect brain chemicals whose
changes, in turn, can contribute to thought, action, actions, and mood disorders. Dementia of the Lewy
Body is one of the most common causes of dementia. LBD diagnostics can be difficult. Symptoms of
Early Lewy body dementia are often confused with related symptoms present in other brain disorders
such as Alzheimer's or schizophrenia in medical settings. Lewy body dementia may also happen
individually or along with other brain diseases.

Symptoms: The symptoms of Lewy Body Dementia includes:

 Thought and reasoning shifts.

 Confusion and alertness differ greatly from day to day or from day to day.
 Slowness, imbalance in gait and other characteristics of Parkinsonian activity.
 Well-formed hallucinations of visuals.
 Deceptions.
 Trouble in visual knowledge interpretation.
 Disruptions in sleep.
 The 'automatic' (autonomic) nervous system malfunctions.
 Loss in recollection, which can be important but less common than Alzheimer's.

Usual age range of onset: Lewy body dementia usually starts at the age of 50 or more, but it is often
encountered by younger individuals. It indicates that LBD impacts significantly more males than females.
Lewy body dementia is a chronic condition, which means that symptoms begin and intensify steadily
over time.

Changes that Occur in Brain: Lewy bodies are composed of alpha-synuclein, a pigment. Alpha-synuclein
plays a variety of important roles in brain neurons (nerve cells) in the healthy brain, especially at
synapses where brain cells associate with each other. Alpha-synuclein develops into clumps within
neurons in Lewy body dementia, beginning in regions of the brain that control facets of memory and
activity. This approach allows neurons to function less efficiently and, inevitably, die. Often impaired are
the functions of such brain chemicals. The effect is extensive disruption to particular brain areas and a
reduction in the skills of certain brain regions.

How the disease typically progresses: Lewy body dementia takes its name from microscopic deposits
found in the brains of persons with the disease. Such deposits cause damage to the nerve cells in the
brain and the subsequent death of them. Lewy body dementia steadily progresses and, like Alzheimer's
disease, continues to advance steadily. Unlike Alzheimer's disease, the concentration and alertness of
the person frequently varies greatly from day to day, even even over the span of a single day, in the
early stages of Lewy body dementia. For those around them, this can also be puzzling.
What current research is being done? : There is a lot to be understood about LBD. Why does
alphasynuclein accumulate in Lewy bodies at a fundamental level, and how do Lewy bodies induce LBD
symptoms? The Alzheimer's and Parkinson's disease research groups are both of growing concern. An
significant link with these other brain diseases is LBD, and research into one condition also leads to
greater knowledge of the others. Many research avenues concentrate on enhancing our understanding
of LBD. Any researchers are working to determine the basic brain variations between Lewy body
dementia and Parkinson's disease dementia. Others look at the basic pathology, physiology, and
environmental risk factors of the disease. Other scientists are also working to identify biomarkers
(biological condition indicators), develop diagnostic screening testing and explore experimental
therapies. Scientists expect that one day, new information about LBD will lead to more successful
therapies and even ways to reverse the condition and avoid it. Before then, for clinical trials, researchers
require volunteers with and without LBD.

5. Alzheimer’s disease
Description: Alzheimer's disease is an irreversible, progressive brain condition that steadily affects the
capacity to accomplish the simplest functions, memory and reasoning skills, and finally. Symptoms first
occur in their mid-60s in most persons of the disease-those with the late-onset form. In a person's 30s to
mid-60s, early-onset Alzheimer's happens and is very rare. The name of the disorder is Dr. Alois
Alzheimer's. Dr. Alzheimer found differences in a woman's brain tissue that had died of an unusual
psychiatric condition in 1906.

Symptoms: In moderate Alzheimer's disease, an individual may appear stable, but it is increasingly
difficult to make sense of the world around him or her. The understanding that something is wrong
always comes to the person and his or her family gradually. Problems can involve:

 Loss in memory
 Poor judgment which leads to poor decisions
 Spontaneity failure and sense of initiative
 Take longer for normal everyday activities to be done
 Questions that echo
 Trouble in money management and paying bills
 Wandering and being confused
 Losing stuff or misplacing it in strange ways
 Shifts of temperament and attitude
 Increased depression and/or violence
Individuals with extreme Alzheimer's do not interact and are solely dependent on others for their
treatment. Near the end, as the body shuts down, the person may be in bed most or all of the time.
Sometimes, their signs include:

 Inability to connect
 The lack of weight
 Convulsions
 Infections of the skin
 Swallowing Trouble
 Groaning, grunting, or crying
 Sleeping rises
 Loss in regulation of the bowels and bladder

Usual age range of onset: Symptoms first begin in their mid-60s among most individuals with
Alzheimer's-those who have the late-onset spectrum. Between a person's 30s and mid-60s, symptoms
of early-onset Alzheimer's begin. The first symptoms of Alzheimer's range from individual to individual.

Changes that Occur in Brain: Usually, the brain shrinks to an extent of healthy aging, but remarkably, in
vast numbers, it does not lose neurons. However, disruption is common in Alzheimer's disease, when
many nerves cease functioning, sever connections with other neurons, and die. Alzheimer's disrupts
mechanisms, including connectivity, digestion, and recovery, that are essential to neurons and their
networks. Initially, nerves and their associations are usually damaged by Alzheimer's disease in areas of
the brain implicated in memory, including the entorhinal cortex and hippocampus. It later influences
regions responsible for vocabulary, reasoning, and social activity in the cerebral cortex. Many more parts
of the brain are gradually affected. A individual with Alzheimer's is slowly losing his or her capacity to
survive and work independently over time. The disease is, ultimately, fatal. In the brain of a person with
Alzheimer's disease, several genetic and cellular changes take place. This modifications can be detected
under the microscope in brain tissue following death. In order to determine which changes may cause
Alzheimer's and which may be the result of the disease, research is underway.

How the disease typically progresses: Alzheimer's disease symptoms worsen over time, but the pace at
which the disease develops varies. On average, a person with Alzheimer's lives four to eight years after
diagnosis, however, depending on other causes, they may live as long as 20 years. Alzheimer's-related
shifts in the brain begin years prior to any symptoms of the disorder. A individual can function
independently in the early stage of Alzheimer's. He or she may also be traveling, working, and being part
of social events. Nevertheless, the person can feel as if he or she has memory lapses, such as missing
familiar phrases or the location of daily things.

The signs of dementia became most severe during the middle stages of Alzheimer's. The individual may
misunderstand terms, get upset or irritated, and behave in unpredictable ways, such as refusing to
bathe. Harm to nerve cells in the brain will also make it impossible for the person without support to
convey thoughts and execute regular tasks.

In the final stage of the disorder, dementia symptoms are serious. Individuals lose the capacity to adapt
to their world, to have a dialogue and, finally, to govern movement. They can sometimes utter phrases
or sentences, but it becomes impossible to express pain. When memories and cognitive capacities begin
to degrade, there could be major personality changes and people require extensive care. 

What current research is being done? : The major research that are currently being done regarding
Alzheimer’s disease are:

 Blood Protein and Lipid Biomarkers for Alzheimer's Disease Diagnosis

 Programmes exploring the role of genetics in the disease of Alzheimer's
 Developing agents that target the enzyme responsible for the production of beta amyloid
selectively
 Diet's role in Alzheimer's Disease prevention
 Identifying and validating peptide agents that neutralize the toxicity of beta amyloid
 Predictive genetic and neuropsychological indicators of cognitive impairment
 Testosterone's role in Alzheimer's Disease

6. Parkinson’s disease
Description: A brain dysfunction that contributes to trembling, weakness, and trouble with walking,
balance, and coordination is Parkinson's disease. Symptoms of Parkinson's generally start off
progressively and get worse over time. People can have trouble walking and talking as the disease
progresses. They may also experience emotional and behavioural changes, issues with sleep, exhaustion,
trouble with memory, and exhaustion.

Symptoms: For various patients, Parkinson's disease signs are different. Some are impossible for even
physicians to detect. Even to an untrained eye, some are visible. If you suspect you're having Parkinson's
symptoms, contact a movement disorder expert. The motor (movement) signs of Parkinson's disease are
typically more common to people (PD). These symptoms are visible from the outside and are used to
create a diagnosis by physicians. PD's three 'cardinal' motor signs are:

 Stiffness
 Slowness
 Resting Tremor

Multiple motor problems can also occur: pacing disorders or balancing and coordination challenges. This
may happen in the process of Parkinson's at any moment, but are more common as the disease
progresses.
The "invisible" signs of Parkinson's are often referred to as non-motor (non-movement) symptoms
because they can not be observed from the outside. These typical symptoms can affect almost any
system of the body, appear at any point during the course of illness (even before motor symptoms or
diagnosis), and vary from person to person in severity. Non-motor effects of patients with Parkinson's
and their families may have a major effect on the quality of life. They can involve:

 Autonomic dysfunction
 Mood and thinking changes
 Other physical changes like drooling, pain, skin changes, etc.

Usual age range of onset: Rarely do young people develop Parkinson's disease. In mid to late life, it
typically starts, and the risk increases with age. About age 60 or older, individuals typically contract the
condition.

Changes that Occur in Brain: A dynamic chain of decisions involving inter-connected groups of nerve
cells called ganglia regulates body activity. Knowledge arrives to a central region of the brain called the
striatum, which acts to transmit signals back and forth from the spinal cord to the brain with the
substantia nigra. It is the duty of the basal ganglia and cerebellum to ensure the motion is carried out in
a steady, flowing way. These signals are transferred from the amygdala to the neuron and travel rapidly
from the brain to the spinal cord and, eventually, to the muscles. In the lack of sufficient activation of
dopamine receptors in the striatum, portions of the basal ganglia are either under- or over-stimulated.
The subthalamic nucleus (STN) becomes overactive, in fact, which serves as a brake on the globus
pallidus interna (GPi), allowing motion and rigidity to shut down. If the GPi is overstimulated, the
thalamus has an over-inhibitory reaction, which in turn inhibits the performance of the thalamus and
induces tremor.

How the disease typically progresses: You may wonder how your illness would unfold if you have
Parkinson's disease (PD). You may like to know what signs you may have, when they're going to start,
and how your life will be impacted. There are questions that are fundamental. Yet Parkinson's disease is
not a simple disorder. In a straight line, it doesn't move, and it's hard to pin down exactly how it will
progress. Parkinson's arrives with two key symptom buckets. One effects the mobility capacity and
contributes to motor disorders such as tremors and stiff muscles. There are non-motor signs on the
other bucket, including pain, lack of smell, and dementia. You do not feel all the symptoms. And you
can't tell how bad they are going to be, or how easily they are going to get worse. Slight tremors but
serious dementia can occur in one person. Another may have severe tremors, but no thought or
memory problems. And there might be someone else with serious signs all over.

What current research is being done? : The major research that are being done are:

 Drug treatments: Drugs that inhibit the activity of glutamate, an amino acid that kills nerve cells,
and the role of the antioxidant coenzyme Q-10 in slowing the development of Parkinson's
disease are being examined by researchers.
 Neural growth factor: Preliminary experiments have shown that the neural growth factor (a
chemical that activates the growth of the nerves) revives the dormant cells needed to generate
dopamine, enhancing symptoms drastically.
 Deep brain stimulation: In order to better explain how deep brain stimulation functions in
Parkinson's disease, study is under way. Scientists are now exploring better methods to activate
the brain.