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Bio Report

The document summarizes key information about Alzheimer's disease (AD). It describes AD as a neurodegenerative disorder characterized by β-amyloid plaques and tau tangles in the brain. AD typically presents as amnestic cognitive impairment affecting short-term memory, but can also impair speech, visuospatial skills, and executive functions. The severity of impairment in AD ranges from mild cognitive impairment to dementia. Caregiver support and managing comorbid conditions like depression are important aspects of AD management and treatment.

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0% found this document useful (0 votes)
25 views9 pages

Bio Report

The document summarizes key information about Alzheimer's disease (AD). It describes AD as a neurodegenerative disorder characterized by β-amyloid plaques and tau tangles in the brain. AD typically presents as amnestic cognitive impairment affecting short-term memory, but can also impair speech, visuospatial skills, and executive functions. The severity of impairment in AD ranges from mild cognitive impairment to dementia. Caregiver support and managing comorbid conditions like depression are important aspects of AD management and treatment.

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kj1576387
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© © All Rights Reserved
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University of central Punjab

Submitted by:
laiba tanveer
Fatima kiani
Zainab daood
Maryam Iqbal

Submitting to:
Prof-QURAT-UL-AIN
TABLE OF CONTENTS
TOPICS PAGE NO
INTRODUCTION 2
FINDINGS 3 AND 4
RECOMMENDATIO 5
NS
SUMMARY 6
REFERENCE 7
INTRODUCTION
Alzheimer disease (AD) is biologically defined by
the presence of β-amyloid-containing plagues and tau-
containing neurofibrillary tangles. AD is a genetic and
sporadic neurodegenerative disease that causes an amnestic
cognitive impairment in its prototypical presentation and
non-amnestic cognitive impairment in its less common
variants. AD is a common cause of cognitive impairment
acquired in midlife and late-life but its clinical impact is
modified by other neurodegenerative and cerebrovascular
conditions. This Primer conceives of AD biology as the brain
disorder that results from a complex interplay of loss of
synaptic homeostasis and dysfunction in the highly
interrelated endosomal/lysosomal clearance pathways in
which the precursors, aggregated species and post-
translationally modified products of Aβ and tau play
important roles. Therapeutic endeavors are still struggling
to find targets within this framework that substantially
change the clinical course in persons with AD.

FINDINGS
The symptoms of Alzheimer's disease progress slowly over several years.
Sometimes these symptoms are confused with other conditions and may
initially be put down to old age.
The rate at which the symptoms progress is different for each individual.

In some cases, other conditions can be responsible for symptoms getting


worse.

These conditions include:

 infections
 stroke
 delirium
As well as these conditions, other things, such as certain medicines, can also
worsen the symptoms of dementia.

Anyone with Alzheimer's disease whose symptoms are rapidly getting worse
should be seen by a doctor so these can be managed.

There may be reasons behind the worsening of symptoms that can be treated.

Generally, the symptoms of Alzheimer's disease are divided into 3


main stages.

In the early stages, the main symptom of Alzheimer's disease is


memory lapses. Someone with early Alzheimer's disease May:

 forget about recent conversations or events


 misplace items
 forget the names of places and objects
 have trouble thinking of the right word
 ask questions repetitively
 show poor judgement or find it harder to make decisions
 become less flexible and more hesitant to try new things
There are often signs of mood changes, such as increasing anxiety or
agitation, or periods of confusion. As Alzheimer's disease develops,
memory problems will get worse. Someone with the condition may find
it increasingly difficult to remember the names of people they know
and may struggle to recognize their family and friends.

 increasing confusion and disorientation – for example, getting


lost, or wandering and not knowing what time of day it is
 obsessive, repetitive or impulsive behavior
 delusions (believing things that are untrue) or feeling paranoid
and suspicious about careers or family members
 problems with speech or language (aphasia)
 disturbed sleep
 changes in mood, such as frequent mood
swings, depression and feeling increasingly anxious, frustrated
or agitated
 difficulty performing spatial tasks, such as judging distances
 seeing or hearing things that other people do not (hallucinations)
Some people also have some symptoms of vascular dementia.

RECOMMENDATIONS
The majority of care and management of
patients with MCI and dementia due to AD (as well as most all-cause MCI and
dementia) occurs in the outpatient setting whilst patients are still living in the
community. Management begins from the first moment of a clinician’s
interaction with patients and their families. Much of the burden of the disease
falls on family caregivers. For most families, having a family member with
cognitive impairment is a novel experience. Compassion, patience and a lack
of condescension are critical to establishing rapport, trust and realistic
expectations. For many, explicit training in this new role may be helpful.
Supporting caregivers is a major mission of the Alzheimer’s Association in the
USA and its sister organizations in other countries. As there are many
uncertainties on how best to deliver caregiver support, there are ongoing
pragmatic trials of the best way to deliver formal care for patients with
dementia. Many patients with cognitive impairment due to AD have
comorbidities that can exacerbate cognitive dysfunction and worsen the
performance of daily activities; of note, many comorbidities may not be
clinically recognized. Patients with concomitant depression or anxiety may
benefit from the use of pharmacological interventions. Treating depression
and anxiety in persons with MCI or dementia due to AD differs from the
treatment of the general population as drugs with an anti-cholinergic
pharmacology should be avoided and lower doses of psychoactive drugs
should be used. Optimizing medication regimens should include minimizing
other psychoactive medications unless clearly indicated. For example,
avoiding medications that induce alterations in gait and balance is a
paramount consideration. Antidepressants such as citalopram or sertraline
may be effective for both anxiety and depression and can be used safely in
patients with cognitive impairment. The treatment of pain in persons with
cognitive impairment is challenging owing to the difficulties that persons with
dementia have in describing their pain.

Summary
Alzheimer disease (AD) is a neurodegenerative disorder characterized by β-
amyloid (Aβ)-containing extracellular plaques and tau-containing intracellular
neurofibrillary tangles. AD typically presents with prominent amnestic
cognitive impairment but can also less commonly manifest as non-amnestic
cognitive impairment. The presentation of AD with short-term memory
difficulty is most common but impairment in expressive speech, visuospatial
processing and executive (mental agility) functions also occurs. Most cases of
AD are not dominantly inherited and there is a complex relationship to
genetics in many persons with AD.

The severity of cognitive impairment in patients with AD varies. The earliest


manifestations can be a subjective decline in mental abilities in the absence of
impaired performance on objective cognitive testing1. Mild cognitive
impairment (MCI) refers to the earliest symptomatic stage of cognitive
impairment in which a single cognitive domain or, possibly, multiple cognitive
domains are impaired to at least a mild extent whilst functional capacities are
relatively preserved. By contrast, dementia is defined as cognitive impairment
of sufficient magnitude to impair independence and affect daily life. Dementia
of gradual onset and ongoing progression with prominent amnestic symptoms
and signs is the prototypical clinical phenotype of AD.

AD was originally considered a clinic pathological entity, meaning that, if the


patient fulfilled the clinical syndrome of an amnestic dementia and other
conditions were ruled out, one could assume that AD pathology was the
cause4. However, increased clinical sophistication together with biomarkers of
AD, namely cerebrospinal fluid (CSF) and PET markers for Aβ and tau, has
transformed the concept of AD to a neurobiological condition that affects
different aspects of cognition. Of note, there is a greater appreciation of the
relationship between AD and other etiologies of cognitive impairment.

Reference
1. Jessen F et al. A conceptual framework for research on subjective cognitive
decline in preclinical Alzheimer’s disease. Alzheimer’s Dement. 10, 844–852
(2014). [PMC free article] [PubMed] [Google Scholar]
2. Petersen RC Mild cognitive impairment as a diagnostic entity. J. Intern. Med 256,
183–194 (2004). [PubMed] [Google Scholar]
3. McKean GM et al. The diagnosis of dementia due to Alzheimer’s disease:
recommendations from the National Institute on Aging and the Alzheimer’s
Association workgroup. Alzheimer’s Dement. 7, 263–269 (2011). [PMC free
article] [PubMed] [Google Scholar]
4. Petersen RC How early can we diagnose Alzheimer disease (and is it sufficient)?
The 2017 Wattenberg lecture. Neurology 91, 395–402 (2018). [PMC free
article] [PubMed] [Google Scholar]
……………………………………………………………………………………..
Report End
Thank you

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