NEUROPSYCHOLOGY ASSIGNMENT

ALZHEIMER’S DISEASE

CASE STUDY
A 63-year-old married man, a right-handed businessman, native of Shanghai, with 12 years of
school education with memory loss and non-fluent speech for 7 years combined with
personality changes for 5 years. The patient recovered from hepatitis A 32 years ago and has
well-controlled hypertension for 30 years.

The patient’s caregiver described that the patient showed forgetfulness and developed poor
pronunciation at the age of 56. His short-term memory has gradually declined as noticed that
he repeatedly gave money to customers while selling clothes. He frequently forgot where he
parked his bicycle, and it was hard for him to speak a full sentence; his language was vague
and short. He was impatient when being asked to repeat a word. Over time, he could only say
some single syllables. He evolved into fully aphasia gradually, and his personality also
changed gradually. At the age of 59, he could not recognise himself in the mirror and he often
hid his shoes because he was worried that they would be stolen. Therefore, his wife had
accompanied him to see a neurologist.

The physical and neurological examination revealed no remarkable signs. His brain MRI
showed mild atrophy in the bilateral frontal lobe. It was revealed that glucose metabolism in
the bilateral frontal and parietal lobe declined, and the left side was significant. The
Mini-Mental State Examination (MMSE) score was 18 out of 30 (18/30). At that point, he
was diagnosed with cognitive impairment and treated with rivastigmine. After the treatment,
his memory improved slightly. In 2017, the neurologist gave him quetiapine and donepezil
due to developing visual hallucinations and irritability. The second brain MRI scan revealed
increased frontal and temporal atrophy compared with the first one.

In May 2019, the patient’s symptoms aggravated further, which included bad temper, crying
often and being more difficult to be looked after. He underwent routine laboratory tests to
exclude non-neurodegenerative and dementia. His neurological examination showed gait
abnormality, negative Babinski’s sign, muscular tension hyperactivity, knee jerk reflex
hyperactivity and a weak positive right palmar jaw reflex. The MMSE score was 3/30. The
patient exhibited severe impairments in orientation (2/10), attention and calculation (1/5),
recall (0/6), language (0/8) and visual construction (0/1). The Montreal Cognitive Assessment
score was 0 (0/30), which was significantly lower than it was in 2015. The third brain MRI
demonstrated atrophy of the cerebral cortex, especially in the bilateral frontal lobes and
hippocampus. The medial temporal lobe atrophy scale was at grade 3.

In addition, three pathogenic genes were tested for early-onset AD related to neurocognitive
disorders, but no mutation was found. A noticeable amyloid deposition in diffuse cortical
areas, particularly in the bilateral frontal, parietal, temporal cortices and posterior cingulated
gyrus was found. Eventually, the diagnosis of frontal variant EOAD was reconfirmed
considering the early onset of dementia, the slow progression of symptoms, the absence of
focal neurological damage signs and the exclusion of other systemic or brain diseases that
could cause dementia. Memantine and donepezil were recommended to improve cognition
and to control psychobehavioural symptoms and vortioxetine to improve mood. After the
treatment and follow-up for 7 months, the patient’s behaviour and mood improved
significally, and his language expression improved slightly.

DEMENTIA
Dementia describes a condition in which there is a gradual, insidious, and relentless loss of
cognitive function. It is the loss of cognitive functioning—thinking, remembering, and
reasoning—and behavioral abilities to such an extent that it interferes with a person’s daily
life and activities. Dementia ranges in severity from the mildest stage, when it is just
beginning to affect a person’s functioning, to the most severe stage, when the person must
depend completely on others for basic activities of daily living.
The DSM-5 gathers all dementia diagnoses into two categories as either major
neurocognitive disorder (NCD) or mild neurocognitive disorder (mild NCD). Major
NCD is defined as “evidence of substantial cognitive decline from a previous level of
performance based upon the concerns of the individual, a knowledgeable informant, or the
clinician; and a decline in neurocognitive performance, typically involving test performance
in the range of two or more standard deviations below appropriate norms on formal testing or
equivalent clinical evaluation” (DSM-5). The cognitive deficits must be sufficient to interfere
with independent functioning and not be attributable to another mental disorder.
Mild NCD is defined similarly, but the DSM-5 stresses a modest cognitive decline from a
previous performance level, a decline in neurocognitive test performance in the range
between one and two standard deviations, and that cognitive deficits do not interfere with
functioning independently.
The most prevalent form of dementia is Alzheimer’s disease. The degenerative disease
Alzheimer’s disease (AD) is the most common cause of dementia.

ALZHEIMER’S DISEASE
Alzheimer’s is a progressive neurodegenerative disease, beginning with mild memory loss
and possibly leading to the loss of the ability to carry on a conversation and respond to the
environment. Alzheimer’s disease involves parts of the brain that control thought, memory,
and language. It can seriously affect a person’s ability to carry out daily activities. Here, the
first problem many people notice is forgetfulness severe enough to affect their ability to
function at home or at work, or to enjoy hobbies. The disease may cause a person to become
confused, get lost in familiar places, misplace things or have trouble with language or the
ability to carry on a conversation and respond to the environment . Alzheimer’s gets worse
over time It can be easy to explain away unusual behavior as part of normal aging, especially
for someone who seems physically healthy. Alzheimer’s is the most common cause of
dementia among older adults.
This damage initially takes place in parts of the brain involved in memory, including the
entorhinal cortex and hippocampus. It later affects areas in the cerebral cortex, such as those
responsible for language, reasoning, and social behavior. Eventually, many other areas of the
brain are damaged.
Alzheimer’s disease is named after Dr. Alois Alzheimer. In 1906, Dr. Alzheimer noticed
changes in the brain tissue of a woman who had died of an unusual mental illness. Her
symptoms included memory loss, language problems, and unpredictable behavior. After she
died, he examined her brain and found many abnormal clumps (now called amyloid plaques)
and tangled bundles of fibers (now called neurofibrillary, or tau, tangles). These plaques and
tangles in the brain are still considered some of the main features of Alzheimer’s disease.
Another feature is the loss of connections between nerve cells (neurons) in the brain. Neurons
transmit messages between different parts of the brain, and from the brain to muscles and
organs in the body

SIGNS AND SYMPTOMS

Signs are externally observable factors, and symptoms are a person’s reported subjective
experiences.

Behavioral
The symptoms of Alzheimer's disease can vary from person to person, but there are common
behavioral signs and symptoms associated with the condition.
● Impaired Judgment: Alzheimer's whatcan lead to poor decision-making and
impaired judgment. This can manifest in situations such as inappropriate financial
decisions or neglecting personal hygiene.
● Mood Changes: Alzheimer's can lead to mood swings and emotional instability.
Individuals may become easily agitated, anxious, or depressed.
● Personality Changes: Some people with Alzheimer's experience changes in
personality. They may become more irritable, suspicious, or withdrawn.
● Loss of Initiative: Individuals may lose interest in activities they once enjoyed and
become passive or apathetic.
● Repetitive Behaviors: Repeating actions, questions, or statements is common in
Alzheimer's patients. This repetition can be frustrating for both the individual and
their caregivers.
● Wandering: People with Alzheimer's may wander aimlessly, often becoming
disoriented and lost. This behavior can pose safety risks.
 ● Difficulty with Daily Tasks: Basic daily tasks, such as dressing, grooming, and
preparing meals, can become increasingly challenging.
● Sleep Disturbances: Alzheimer's can disrupt sleep patterns, leading to increased
nighttime wakefulness and daytime sleepiness.
Psychological
Alzheimer's disease is primarily characterized by cognitive and behavioral symptoms, but it
can also lead to psychological symptoms. These psychological symptoms can be challenging
for both individuals with Alzheimer's and their caregivers. Some common psychological
symptoms associated with Alzheimer's disease include:
● Depression: Many individuals with Alzheimer's experience depression, which can
manifest as persistent sadness, withdrawal from activities, changes in appetite or
weight, and feelings of hopelessness.
● Anxiety: Anxiety is common in Alzheimer's patients and can lead to restlessness,
excessive worry, irritability, and even physical symptoms such as trembling or
sweating.
● Paranoia : Some individuals with Alzheimer's develop paranoid thoughts and beliefs,
such as believing that others are stealing from them or plotting against them.
● Agitation and aggression: Agitation involves restlessness, pacing, and sometimes
verbal or physical aggression. It can be triggered by confusion, frustration, or
environmental factors.
● Apathy: Apathy is a common psychological symptom in Alzheimer's and can
manifest as a lack of interest in activities, social withdrawal, and reduced motivation.
● Hallucinations and Delusions: In the later stages of Alzheimer's, some individuals
may experience hallucinations (seeing or hearing things that are not there) or
delusions (false beliefs).
● Emotional Lability: Emotional lability involves rapid and exaggerated mood swings,
where a person can shift between emotions like sadness, anger, and happiness
relatively quickly.
● Euphoria: In some cases, individuals with Alzheimer's may exhibit unwarranted
euphoria, appearing overly cheerful or happy even in inappropriate situations.
● Sexual Inappropriateness: Alzheimer's can lead to changes in social behavior,
including sexual disinhibition and inappropriate comments or actions.

Cognitive
Alzheimer’s slow onset and steady progress are its most insidious features, gradually robbing
a person first of recent memory, then of more remote memory, and finally of the abilities to
recognize family members and to function independently. Disease progress is gradual:
patients spend months to years in each of several progressive stages ranging from mild to
severe impairment.

Impairments span five measures of cognitive function: concentration, recent and past
memory, orientation, social functioning, and self-care (see, e.g., Reisberg, 1983).

Memory problems are typically one of the first signs of cognitive impairment related to
Alzheimer’s disease. Some people with memory problems have a condition called mild
cognitive impairment (MCI). In MCI, people have more memory problems than normal for
their age, but their symptoms do not interfere with their everyday lives. Movement
difficulties and problems with the sense of smell have also been linked to MCI. Older people
with MCI are at greater risk for developingAlzheimer’s, but not all of them do. Some may
even go back to normal cognition
The more marked deficits in memory include:
● An inability to recall autobiographical information from long-term memory
(information about people, events and conversations, for example), the major
characteristic of the disease and one that appears early in the disorder development
(Greene and Hodges 1996a; Fleishman and Gabrieli 1999)
● Impaired recall of previously learned information and, sometimes, memory for
conceptual or factual information;
● Rapid forgetting;
● Explicit memory impairment (implicit memory is relatively preserved);
● Short- and long-term memory impairment (Fleishman and Gabrieli 1998);
● Tendency to show a lack of a primacy effect but show a recency effect – patient will
more correctly recall items from the end of a list than the beginning (Bayley et al.
2000);
● Interference by previously learned information when new material is learned;
● Attention and working memory impairment;
● Semantic memory impairment – inability to recall over-learned information;
● Circumlocution and paraphrasic errors;
● Delayed-memory impairment – this appears to be best at discriminating DAT patients
from controls (Zakzanis et al. 1999).
The first symptoms of Alzheimer’s vary from person to person. For many, decline in non-
memory aspects of cognition, such as word-finding, vision/spatial issues, and impaired
reasoning or judgment, may signal the very early stages of Alzheimer’s disease.
Researchers are studying biomarkers (biological signs of disease found in brain images,
cerebrospinal fluid, and blood) to see if they can detect early changes in the brains of people
with MCI and in cognitively normal people who may be at greater risk for Alzheimer’s
disease. Studies indicate that such early detection may be possible, but more research is
needed before these techniques can be relied upon to diagnose Alzheimer’s disease in
everyday medical practice.

Cummings and Benson (1992) suggest that AD develops in three stages.

I. In the first stage (within three years), memory for recent (and some remote) events is
impaired. New learning is impaired. Spatial perception declines, disorientation in time
and place occurs and concentration is impaired. The patient feels fatigued, restless,
apathetic and sometimes sad. There is impaired verbal fluency and mild anomia.
II. In the second stage (within two to ten years), memory failure progresses, with
impaired recent and remote memory recall, and parietal lobe dysfunction such as
dyspraxia and agnosia occur. Judgement and the capacity for abstract thought
disappear. Patients are anomic and have difficulty understanding speech.
III. In the third and final stage (between eight and twelve years), all intellectual function
breaks down. Gross emotional disinhibition and disorientation occurs, and the former
personality is lost. Patients reach the stage where they cannot recognize relatives, or
even recognize themselves in a mirror. Behaviourally, DAT patients may be socially
withdrawn and apathetic, and depression is a commonly experienced disorder. There
may be paranoia and examples of the misidentification syndrome – believing a carer
is an impostor.

DIAGNOSTIC CRITERIA
The DSM-5 diagnostic criteria for Major or Mild Neurocognitive Disorder Due to
Alzheimer’sDisease, it states that -
A. The criteria are met for major or mild neurocognitive disorder.
 B. There is insidious onset and gradual progression of impairment in one or more
cognitive domains (for major neurocognitive disorder, at least two domains must be
impaired).
C. Criteria are met for either probable or possible Alzheimer’s disease as follows:
For major neurocognitive disorder:
Probable Alzheimer’s disease is diagnosed if either of the following is present; otherwise,
possible Alzheimer’s disease should be diagnosed.
1. Evidence of a causative Alzheimer’s disease genetic mutation from family history or
genetic testing.
2. All three of the following are present:
a. Clear evidence of decline in memory and learning and at least one other
cognitive domain (based on detailed history or serial neuropsychological
testing).
b. Steadily progressive, gradual decline in cognition, without extended plateaus.
c. No evidence of mixed etiology (i.e., absence of other neurodegenerative or
cerebrovascular disease, or another neurological, mental, or systemic disease
or condition likely contributing to cognitive decline).
For mild neurocognitive disorder:
Probable Alzheimer’s disease is diagnosed if there is evidence of a causative Alzheimer’s
disease genetic mutation from either genetic testing or family history. Possible Alzheimer’s
disease is diagnosed if there is no evidence of a causative Alzheimer’s disease genetic
mutation from either genetic testing or family history, and all three of the following are
present:
1. Clear evidence of decline in memory and learning.
2. Steadily progressive, gradual decline in cognition, without extended plateaus.
3. No evidence of mixed etiology (i.e., absence of other neurodegenerative or
cerebrovascular disease, or another neurological or systemic disease or
condition likely contributing to cognitive decline).
D. The disturbance is not better explained by cerebrovascular disease, another
neurodegenerative disease, the effects of a substance, or another mental, neurological,
or systemic disorder.
If the diagnosis is Alzheimer’s, beginning treatment early in the disease process may help
preserve daily functioning for some time, even though the underlying disease process cannot
be stopped or reversed. An early diagnosis also helps families plan for the future. They can
take care of financial and legal matters, address potential safety issues, learn about living
arrangements, and develop support networks. In addition, an early diagnosis gives people
greater opportunities to participate in clinical trials that are testing possible new treatments
for Alzheimer’s disease or other research studies.

ONSET
For most people with Alzheimer’s — those who have the late-onset variety — symptoms first
appear in their mid-60s or later. When the disease develops before age 65, it’s considered
early-onset Alzheimer’s, which can begin as early as a person’s 30s, although this is rare.

The onset of symptoms is usually in the eighth and ninth decades; early-onset forms seen in
the fifth and sixth decades are often related to known causative mutations. Symptoms and
pathology do not differ markedly at different onset ages.

COURSE OF DISORDER -

Major or mild NCD due to Alzheimer's disease progresses gradually, sometimes with brief
plateaus, through severe dementia to death. The mean duration of survival after diagnosis is
approximately 10 years, reflecting the advanced age of the majority of individuals rather than
the course of the disease; some individuals can live with the disease for as long as 20 years.
Changes in the brain related to Alzheimer's begin years before any signs of the disease. This
time period, which can last for years, is referred to as preclinical Alzheimer's disease.

Late-stage individuals are eventually mute and bedbound. Death most commonly results from
aspiration in those who survive through the full course. In mild NCDs due to Alzheimer's
disease, impairments increase over time, and functional status gradually declines until
symptoms reach the threshold for the diagnosis of major NCD.

However, younger individuals are more likely to survive the full course of the disease, while
older individuals are more likely to have numerous medical comorbidities that affect the
course and management of the illness. Diagnostic complexity is higher in older adults
because of the increased likelihood of comorbid medical illness and mixed pathology.

RISK FACTORS
Age- The greatest known risk factor for Alzheimer’s and other dementias is increasing age,
but these disorders are not a normal part of aging. While age increases risk, it is not a direct
cause of Alzheimer's. Most individuals with the disease are 65 and older. After age 65, the
risk of Alzheimer's doubles every five years. After age 85, the risk reaches nearly one-third.

Family history- Another strong risk factor is family history. Those who have a parent,
brother or sister with Alzheimer’s are more likely to develop the disease. The risk increases if
more than one family member has the illness. When diseases tend to run in families, either
heredity (genetics), environmental factors, or both, may play a role.

Genetics (heredity)- Scientists know genes are involved in Alzheimer’s. Two categories of
genes influence whether a person develops a disease: risk genes and deterministic genes.
Alzheimer's genes have been found in both categories. It is estimated that less than 1% of
Alzheimer’s cases are caused by deterministic genes (genes that cause a disease, rather than
increase the risk of developing a disease).

Down's syndrome- People with Down's syndrome are at a higher risk of developing
Alzheimer's disease. This is because the genetic changes that cause Down's syndrome can
also cause amyloid plaques to build up in the brain over time, which can lead to Alzheimer's
disease in some people.

Head injuries- People who have had a severe head injury may be at higher risk of
developing Alzheimer's disease, but much research is still needed in this area.

Cardiovascular disease- Research shows that several lifestyle factors and conditions
associated with cardiovascular disease can increase the risk of Alzheimer's disease.These
include:
● Smoking
● Obesity
● Diabetes
● high blood pressure
● high cholesterol

Other risk factors- In addition, the latest research suggests that other factors are also
important, although this does not mean these factors are directly responsible for causing
dementia. These include:
● hearing loss
 ● untreated depression (though depression can also be one of the symptoms of
Alzheimer's disease)
● loneliness or social isolation
● a sedentary lifestyle

CAUSES OF ALZHEIMER
Immune Reactions - Some researchers think that in old age the immune system loses its
ability to recognize a person’s own body. As a result, it develops antibrain antibodies that
cause neuronal degeneration. In other words, the body actually begins to kill its own neurons,
which leads to dementia.

Blood Flow - Historically, Alzheimer’s disease was attributed to poor circulation. In healthy
people, blood flow to the brain declines by more than 20 percent between the ages of 30 and
60, but the brain compensates by more-efficient oxygen uptake. In Alzheimer’s disease, the
decline is enhanced, but there are no compensatory mechanisms. The greatest decreases in
blood flow are found in those brain areas in which the most degenerative change is seen.
What is not known is whether the declines in blood flow and glucose metabolism are causal
or secondary to degenerative brain changes.

Neuritic (Amyloid) Plaques - Neuritic plaques, also known as senile plaques, are found
chiefly in the cerebral cortex and result from the accumulation of tau protein. Their increased
concentration in the cortex has been correlated with the magnitude of cognitive deterioration.
Neuritic plaques are generally considered nonspecific phenomena in that they can be found in
non-Alzheimer patients and in dementias caused by other known events.

Paired Helical Filaments - Also known as neurofibrillary tangles, paired helical filaments
are found in both the cerebral cortex and the hippocampus and are believed to be related to
the tau protein. The posterior half of the hippocampus is affected more severely than the
anterior half. They have been described mainly in human tissue and have been observed not
only in patients with Alzheimer’s disease but also in patients with Down syndrome,
Parkinson’s disease, and other dementias.
Neocortical Changes - The neocortical changes are not uniform. Although the cortex
shrinks, or atrophies, losing as much as one-third of its volume as the disease progresses. The
darker the red, the more severe the degeneration.

Paralimbic Cortex Changes - The limbic system undergoes the most severe degenerative
changes in Alzheimer’s disease, and of the limbic structures, the entorhinal cortex is affected
earliest and most severely. Damage to the entorhinal cortex is associated with memory loss,
and given that memory loss is an early and enduring symptom of the disease, it is most likely
caused by the degenerative changes that take place in this limbic area.

Abnormal deposits of proteins form amyloid plaques and tau tangles throughout the brain.
Once healthy neurons stop functioning and lose connections with other neurons, they die. The
damage initially appears to take place in the hippocampus, the part of the brain essential to
forming memories. As more neurons die, additional parts of the brain are affected, and they
begin to shrink. By the final stage of Alzheimer’s, damage is widespread and brain volume
has shrunk significantly.
Scientists don’t yet fully understand what causes Alzheimer’s disease in most people. In
people with early-onset Alzheimer’s, a genetic mutation is usually the cause. Late-onset
Alzheimer’s arises from a complex series of brain changes that occur over decades. The
causes probably include a combination of genetic, environmental, and lifestyle factors. The
importance of any one of these factors in increasing or decreasing the risk of developing
Alzheimer’s may differ from person to person

Health, Environmental, and Lifestyle Factors Research suggests that a host of factors beyond
genetics may play a role in the development and course of Alzheimer’s disease. There is a
great deal of interest, for example, in the relationship between cognitive decline and vascular
conditions such as heart disease, stroke, and high blood pressure, as well as metabolic
conditions such as diabetes and obesity. Ongoing research will help us understand whether
and how reducing risk factors for these conditions may also reduce the risk of Alzheimer’s. A
nutritious diet, physical activity, social engagement, and mentally stimulating pursuits have
all been associated with helping people stay healthy as they age. These factors might also
help reduce the risk of cognitive decline and Alzheimer’s disease. Clinical trials are testing
some of these possibilities.

PREVALENCE
The prevalence of overall dementia (major NCD) rises steeply with age. In high-income
countries, it ranges from 5% to 10% in the seventh decade to at least 25% thereafter. U.S.
census data estimates suggest that approximately 7% of individuals diagnosed with
Alzheimer's disease are between ages 65 and 74 years, 53% are between ages 75 and 84
years, and 40% are 85 years and older. The percentage of dementias attributable to
Alzheimer's disease ranges from about 60% to over 90%, depending on the setting and
diagnostic criteria. An estimated 6.7 million Americans age 65 and older are living with
Alzheimer's in 2023. Seventy-three percent are age 75 or older. About 1 in 9 people age 65
and older (10.7%) has Alzheimer's.
In the year 2019, India was estimated to have ~3.69 million active cases of AD and other
dementias. A prevalence rate of 4.3% for AD and other dementias in India was reported.

COMORBIDITY
Most individuals with Alzheimer's disease are elderly and have multiple medical conditions
that can complicate diagnosis and influence the clinical course. Major or mild NCD due to
Alzheimer's disease commonly co-occurs with cerebrovascular disease, which contributes to
the clinical picture. When a comorbid condition contributes to the NCD in an individual with
Alzheimer's disease, then NCD due to multiple etiologies should be diagnosed.
Alzheimer’s disease (AD) is often associated with a wide range of comorbid diseases such as
hypertension, osteoarthritis, depression, diabetes, and cerebrovascular disease. An increased
risk of mortality with comorbidities, such as cardiovascular disease, diabetes, and stroke have
been reported in people with AD, while other studies have not found increased risk with these
comorbidities.

PROGNOSIS
Alzheimer’s disease life expectancy is an average of 3 to 11 years after diagnosis. However,
some people can live 20 years or longer after they are diagnosed. Prognosis usually depends
on the person’s age and how much the condition has progressed before diagnosis..

There is no known cure for Alzheimer's disease; the disease naturally progresses and worsens
over time. People with the disease can survive for many years, however. Some people decline
steadily during their disease, while others reach major plateaus where their symptoms
advance quite slowly. Men and people with a long-standing history of high blood pressure are
more likely to decline rapidly. Additionally, the older a person with Alzheimer's disease
becomes, the more likely he or she is to decline rapidly. An accurate, early diagnosis gives
affected individuals a greater chance of benefiting from existing treatments.

Death can occur as a result from other conditions that result from the complications of
Alzheimer’s disease. For example, when Alzheimer’s disease affects a person’s ability to
swallow, he or she can become dehydrated, suffer malnutrition, or develop aspiration
pneumonia if food and drink goes into the airways.

DIFFERENTIAL DIAGNOSIS

Other neurocognitive disorders- Major and mild NCDs due to other neurodegenerative
processes (e.g., Lewy body disease, frontotemporal lobar degeneration) share the insidious
onset and gradual decline caused by Alzheimer's disease but have distinctive core features of
their own. In major or mild vascular NCD, there is typically history of stroke temporally
related to the onset of cognitive impairment, and infarcts or white matter hyperintensities are
judged sufficient to account for the clinical picture. However, particularly when there is no
clear history of stepwise decline, major or mild vascular NCD can share many clinical
features with Alzheimer's disease.
Other concurrent, active neurological or systemic illness. Other neurological or systemic
illness should be considered if there is an appropriate temporal relationship and severity to
account for the clinical picture. At the mild NCD level, it may be difficult to distinguish an
Alzheimer's disease etiology from that of another medical condition (e.g., thyroid disorders,
vitamin Bj2 deficiency).
Major depressive disorder. Particularly at the mild NCD level, the differential diagnosis
also includes major depression. The presence of depression may be associated with reduced
daily functioning and poor concentration that may resemble an NCD, but improvement with
treatment of depression may be useful in making the distinction.

TREATMENT OF ALZHEIMER ’S DISEASE

Alzheimer’s disease is complex, and it is unlikely that any one drug or other intervention will
successfully treat it. Current approaches focus on helping people maintain mental function,
manage behavioral symptoms, and slow or delay the symptoms of disease.
Researchers hope to develop therapies targeting specific genetic, molecular, and cellular
mechanisms so that the actual underlying cause of the disease can be stopped or prevented.
Alzheimer’s disease research has developed to a point where scientists can look beyond
treating symptoms to think about addressing underlying disease processes. In ongoing clinical
trials, scientists are developing and testing several possible interventions, including
immunization therapy, drug therapies, cognitive training, physical activity, and treatments
used for cardiovascular disease and diabetes. Some caregivers have found that joining a
support group is a critical lifeline. These support groups allow caregivers to find respite,
express concerns, share experiences, get tips, and receive emotional comfort. Many
organizations sponsor in-person and online support groups, including groups for people with
early-stage Alzheimer’s and their families.

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