Alzheimer_TOC sample.pdf

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AnejoHe

althCommunications

Margaret Bray


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Margaret Bray


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// Pocket Guide to Alzheimers Disease

Table of Contents


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Treating Alzheimers Disease. Cholinesterase Inhibitors. NMDA Receptor Antagonist, MemantineTreatment of Associated Conditions

.Treatments for Behavioral Symptoms.Treating Sleep Problems.Alternative Therapies. Ginkgo Biloba.Vitamin E

. Fatty Acids and Lipids. Omega-3 fatty acids. Caprylic Acid and Coconut oil. Phosphatidylserine

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IntroductionAlzheimer disease (AD) is the most common cause of dementia in


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three copies rather than two. Indeed, many individuals with Downs

syndrome develop Alzheimer's disease, often as young as their 30s and 40s.It has also been shown that people with the apolipoprotein E4

(ApoE4) gene (approximately 1 in 7 of the population in the US) are

at higher risk for developing Alzheimer's disease. It is believed ApoE4

attaches itself to a brain cell receptor, that in turn attaches to APP, and

is carried into the brain cell, where proteases breakdown APP producingprotein fragments (beta-amyloid) that are believed to be the start of

the cause of degeneration and death of neurological tissue, and the

manifestation of the characteristics of Alzheimers disease. Research

is ongoing to identify further possible routes and causes of the disease.

Healthy Neuron


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In 1901 Alois Alzheimer described what we now believe to be

Alzheimers disease in a 51-year-old woman named Auguste Deter.

Alzheimer diagnosed Deter with presenile dementia, which today

It was in 1906 that a German physician, Alois Alzheimer, recorded

brain cell abnormalities while performing an autopsy on a patient whohad died after years of severe memory problems, confusion and difficulty

understanding questions. While performing a brain autopsy, Alzheimer

noted dense deposits surrounding the nerve cells (neuritic plaques)

and inside the nerve cells he observed twisted bands of fibers (neurofibrillary

tangles). Today, when these plaques and tangles are found during autopsythere is certain diagnosis of Alzheimer's disease. Despite knowledge

of the underlying pathology, treatments that directly target the underlying

molecular pathways and halt the brain degeneration, specifically the formation

of plaques and tangles, have still to be identified, although progress has

been made in this field (2010 Progress Report on Alzheimers Disease).


8/28More recent tissue section showing plaques and tangles


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Today the only approved treatments for Alzheimers are those thathave an indirect effect through the slowing of cognitive decline by aiding

neurotransmission. These drugs include the cholinesterase inhibitors

(donepezil, galantamine and rivastigmine), whose mode of action is

to make more acetylcholine available for neural communication processes

in otherwise deteriorating cells, and the N-methyl-D-aspartate(NMDA) receptor antagonist, memantine. These drugs do not delay

or halt progression of the disease, but help to maintain neurotransmission

across brain cells, provide temporary symptomatic relief and may slow

symptoms of cognitive decline in mainly in the earlier stages of

Alzheimers disease.

In this book we describe as much as possible that is known about

Alzheimers disease today, from the possible causes and risk factors,

through diagnosis, treatments and advances in the understanding of

the disease.


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There is no single test that can show whether a person has Alzheimer's.

Furthermore, it has become increasingly evident that the signs and

Diagnostic TestsDiagnosis


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Sample MMSE questions

1. Orientation to time: 'What is the date?'

2. Registration: 'Listen carefully. I am going to say three words. You

say them back after I stop. Ready? Here they are... apple [pause], penny

[pause], table [pause]. Now repeat those words back to me.' [Repeat

up to 5 times, but score only the first trial.]3. Naming: 'What is this?' [Point to a pencil or pen.]

4. Reading: 'Please read this and do what it says.' [Show examinee the

following words on the stimulus form]: Close your eyes

As well as routine laboratory tests, biomarkers can be measured help

rule out other causes of dementia, for example, ApoE4 testing, but

these tests are not routine. Genetic testing for ApoE4 or for familial

(source: http://alzheimers.org.uk)


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1.

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3.

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Memory loss that disrupts daily life

Challenges in planning or solving problems

Difficulty completing familiar tasks at home, at work or at leisure

Confusion with time or place

Trouble understanding visual images and spatial relationships

New problems with words in speaking or writing

Misplacing things and losing the ability to retrace steps

Decreased or poor judgment

Withdrawal from work or social activities

Changes in mood and personality

The Alzheimers Association (2009)10 warning signs of Alzheimers disease


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New Diagnostic Criteriaand Guidelines for

Alzheimer's DiseaseThe original clinical criteria for diagnosing Alzheimer's disease were


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Now for the first time in nearly 30 years, the clinical diagnostic criteria

for Alzheimer's disease dementia have been revised.Expert international workgroups convened by the Alzheimer's Association

and the National Institute of Aging (NIA) have jointly issued four new

criteria and guidelines to diagnose Alzheimer's disease. These new criteria

update, refine and broaden previous widely used guidelines jointly issued

by the Alzheimer's Association and the National Institute of Health(NIH) over the past 30 years (Jack et al, 2011).The final versions of

the guidelines, revised to reflect input from the professional community

at large, now appear as free-access papers in Alzheimer's and Dementia:

The Journal of the Alzheimer's Association [abbreviated, Alzheimers

Dement] (Albert et al, 2011; Jack et al, 2010; McKhann et al, 2011;

Sperling et al, 2011). The new guidelines aim to improve current diagnosis,

strengthen autopsy reporting of Alzheimer's brain changes, and establish

a research agenda for future progress in earlier detection and even greater

diagnostic accuracy


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Alzheimer's disease progression

EARLIEST ALZHEIMERS

changes may begin years or

more before diagnosis.


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ABNORMAL

NORMAL

TIM

Pre-Symptomatic eMCI lMCI Dementia

CSFabeta 42

CSF A42

MRI Hippocampal Volume

FDG-PET

Amyloidimaging

FxnCogCSF tau

MRI hipp

Alzheimers Disease Progression


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Summary of New Diagnostic Criteria and

Guidelines for Alzheimers DiseaseDementia due to Alzheimer's Disease

Clinical symptom of dementia due to Alzheimer's disease are impairments

in memory, thinking and behavior decrease a person's ability to functionindependently in everyday life (McKhann et al, 2011). The dementia due

to Alzheimer's disease guideline updates and clarifies clinical criteria to

diagnose dementia from all causes and specifically from Alzheimer's

disease (McKhann et al, 2011). In the future, biomarker evidence may

provide additional diagnostic certainty.

The dementia due to Alzheimers as outlined in the new guidelines is

further categorised into three sub-criteria:


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Mild Cognitive Impairment (MCI) due to

Alzheimer's Disease

Symptoms of MCI due to Alzheimer's disease are noticible mild changes

in memory and thinking that can be measured on mental status tests,

but are not severe enough to disrupt a person's day-to-day life (Albert et

al, 2011).The new guideline for MCI due to Alzheimer's disease is based on two

sets of criteria:

Core clinical criteria clinical and cognitive assessments that establish

concern of change in cognition over time; impairment in 1 or more

cognitive domain; preservation of independence in functional abilities;

not demented, and etiologyof MCI consistent with Alzheimers,

including where relevant, Alzheimers genetic factors. Core clinical

criteria can be used in clinical settings.

Research criteria incorporates biomarkers advanced imaging and

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may best confirm that Alzheimer's-related changes are underway and

how best to measure them. These preclinical guidelines are also notmeant to imply that all individuals with early Alzheimers pathology

will progress to clinical Alzheimers dementia. Furthermore, although

changes in CSF levels of the three most common known protein markers

(beta-amyloid, tau and phosphorylated tau) may be measured reliably

in the controlled trial setting, individuals vary greatly in the rates atwhich they develop signs and symptoms of Alzheimer's; presently,

brain structural changes are a more reliable method that CSF markers

in predicting cognitive decline.

The newly defined preclinical stage of Alzheimer's may also help in

the search for new treatments. Further they could help optimize currenttreatment strategies and help define when best to start treatment in

the early course of this deliberating disease.

Biomarkers


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impairment; an "ABC" score for neuropathologic change that incorporates

histopathologic assessments of amyloid deposits (A), staging ofneurofibrillary tangles (B), and scoring of neuritic plaques (C); and a

more detailed approaches for assessing commonly co-morbid conditions

such as Lewy body disease, vascular brain injury, hippocampal sclerosis,

and TAR DNA binding protein (TDP)-43 immunoreactive inclusions

(Montine et al, 2012). As with the other guidelines, the neuropathologicguidelines recommend use of biomarker data to complement autopsy

findings to help advance understanding of how closely biomarkers

correlate with the underlying physical processes.

Brain scans help identify Alzheimers


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Neurofibrillary tangles

Apoptosis

AberrantNeuronal

Death Hyperphosphorylationof Tau

AICDROS

Formation

Activation of PKC,PKA, ERK2

Alzheimers Disease StateNormal State



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Anejo Health Communications

ISBN: 978-950-9647-78-7

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