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INTERGRATED STUDIES IN MENTAL HEALTH > Dementia and Alzheimer's disease jerome > Flashcards

Dementia and Alzheimer's disease jerome Flashcards

1
Q

what is the definition of dementia

A

Syndrome which refers to

  • progressive decline in intellectual functioning (COGNITION), severe enough to interfere with person’s normal daily activities and social relationships.
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2
Q

which age group is affected by dementia

A

over 65, and likelihood increases with ae

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3
Q

what is the statistics of people diagnosed with dementia for the age of 60 and 80

A

age 60: 1 in 20

age 80: 1 in 5

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4
Q

list the most prevalent forms of dementia

A

Alzheimer’s Disease
Vascular Dementia
Lewy Body Dementia
Frontotemporal

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5
Q

list the rarer forms of dementia

A

pre-senile Dementia
Picks Disease
Korsakov Dementia*
Pseudo-dementia*
Endocrine related Dementia*
Parkinson’s Disease
Huntington’s chorea
Posterior cortical atrophy
Normal Pressure Hydrocephalus*
Neurosyphilis*

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6
Q

what does vascular dementia refer to

A

it refers to the pathology and it is an umbrella term that refers to many different types

this dementia mainly resides in some of the blood vessels located within the brain and neurones in the brain

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7
Q

what is the stepwise progression of vascular dementia

A

Cerebral amyloid angiography - build up of amyloid beta protein within the blood vessels. this impairs the blood supply to certain brain regions.

over the course of a lifetime, the neurones die

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8
Q

what are the symptoms of vascular dementia

A

> memory difficulties
executive difficulties

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9
Q

What do patients with vascular dementia have history of

A

stroke and falls

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10
Q

what are the risk factors of vascular dementia

A

High blood pressure, high cholesterol, diabetes

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11
Q

what is lewy body dementia

A

it is under umbrella of disease related to parkinsons disease

refers to underlying pathology

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12
Q

what are lewy bodies

A

insoluble aggregates of certain proteins, most importantly alpha synuclein

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13
Q

what are the early symptoms of lewy body dementia

A

executive difficulties, visuospatial problems, hallucinations

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14
Q

what is frontotemporal dementia

A

it is an umbrella term for dementia in the frontal temporal lobe such as Picks disease, semantic dementia , primary progressive aphasia (PPA)

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15
Q

what are the main cognitive deficits of fronto temporal dementia

A

> executive functioning
attention

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16
Q

what are the 3 changes in cognitive symptoms with dementia

A

perception
executive functioning
language

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17
Q

what is perception

A

the process of making sense of information externally (environment) and internally ( your body)

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18
Q

what happens in loss of perception

A

> unable to recognise objects

> unable to judge the position / location of people and objects

> ignoring one side of the world (including oneself and environment)

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19
Q

what is executive functioning

A

processing of information in order to plan, sequence, make decisions, prioritize, problem-solve and self-monitor

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20
Q

what happens during loss of executive functioning

A

> difficulties initiating tasks

> getting stuck on tasks / repeating actions

> not thinking through consequences of actions

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21
Q

what is language

A

understanding information said by others (receptive language) and the process of expressing information (expressive language)

22
Q

what happens in loss of language

A

> difficulties understanding

> difficulties finding the word

> reduced vocabulary

23
Q

what are the 3 changes in cognitive symptoms with dementia

A

perception
excecutive functioning
language

24
Q

what are the non cognitive symptoms of dementia

A

Apathy / Indifference

Disinhibition

Irritability / lability / aggression

Aberrant motor behaviour

Night-time behaviour

Appetite / Eating change

Delusions

Hallucination

Agitation / wandering

Depression / dysphoria

Anxiety

Euphoria/elation

25
Q

what is the MMSE

A

Mini mental state exam (MMSE)

  • a series of questions and tests
  • tests a number of different mental abilities ( memory , attention , language )
26
Q

How is dementia clinically diagnosed

A

patient need to show:

1, memory impairment

  1. impairment in one of the following : language, motor activity, recognition, executive functioning
  2. continuing cognitive decline
27
Q

what is the histopathophysiology of Alzheimer disease (AD) ( inside and outside neurones)

A

based on 2 proteins:

  1. amyloid plaques - outside the neurones
  2. neurofibrillary tangles - inside the neurones
28
Q

what is amyloid plaques

A

they occur when large amounts of a 42 amino acid peptide termed B-amyloid (beta amyloid) or AB42b, clunk together to form a plaque

29
Q

why is amyloid plaques difficult to remove by the brain

A

they are insoluble

30
Q

what is neurofibrillary tangles

A

they are rich in cytoskeletal proteins, especially the microtubule- associated protein “tau”

31
Q

what are in the tangles of neurofibrillary tangles

A

heavily phosphorylated proteins which may cause aggregation and precipitation of the cytoskeleton

32
Q

why is this histopathophysiology of AD proposed

A

they found these plaques and tangles post mortem so they assumed that if these pathology are only present in the Alzheimer brain then Alzheimer is the result of them

33
Q

what do you have to consider with the proposed histopathophysiology of AD

A

that the amyloid plaques and tangles are a consequence of Alzheimer’s and not the driving cause

34
Q

what are the 2 major hypothesis of AD

A
  1. BAPtists - Beta amyloid protein
  2. TAUists - TAU
35
Q

what is the BAPtists hypothesis of AD

A

The accumulation of a fragment of the amyloid precursor protein [APP] (the amyloid beta 42 residue fragment or Ab-42) leads to the formation of plaques that kill neurons.

36
Q

what is the TAUist hypothesis of AD

A

Abnormal phosphorylation of tau proteins makes them “sticky,” leading to the break up of microtubules. The resulting loss of axonal transport causes cell death.

37
Q

What is Amyloid precursor protein (APP) thought to be important for

A

neuronal growth, survival and repair

38
Q

what is the evidence for the Beta amyloid protein hypothesis

A
  1. The amyloid precursor protein (APP) is broken down by a series of secretases.
  2. During this process, a non-soluble fragment of the APP protein (called Ab-42) accumulates and is deposited outside the cell.

3.The non-soluble or “sticky” nature of Ab-42 helps other protein fragments(including apoE) to gather into plaques.

4.Somehow the plaques (or possible the migration of Ab-42 outside the cell) cause neuronal death.

39
Q

what is the evidence for the TAU hypothesis

A
  • Neurons have an internal support structure partly made up of microtubules.
  • A protein called tau helps stabilize microtubules by acting as a 3d “rail road tide” for the microtubule
  • In AD, tau changes, causing microtubules to collapse, and tau proteins clump together to form neurofibrillary tangles (NFTs).
  • These neurofibrillary tangles are a result of an accumulation of paired helical filaments (PHF) caused by accumulation of phosphate on the tau proteins. PHFs are the main component of NFTs
40
Q

what are the current theories of AD

A

that AD is multifactorial: 1. involves several pathways and pathology, 2. dependent on life experience such as trauma, exposure to toxicants

  1. protein accumulation: Beta plaques and Tau tangles : does not fully explain all of the pathology
  2. induces inflammation: overactive brain immune cells (microglia)
  3. this affects the energy processing of neurons, resulting in oxidative stress: development of free radicles with lead to neuronal death
41
Q

why is it hard to develop a treatment for AD

A

its several pathways and pathology.

42
Q

how many stages of AD are there and what do they mean

A

3 stages and they each correlate with the clinical symptoms and onset of pathology

stage 1: preclinical / mild cognitive impairment
stage 2: moderate
stage 3:

43
Q

In stage 1 of AD (preclinical to mild) where are the histopathology signs of AD noticed

A

so overall brain is normal, normal amount of cerebral cortex, brain matter and white matter, however you start to see TAU tangles and neuronal death in the regions below:

  1. Brainstem (noradrenergic neurons)
  2. cholinergic neurons - decreased brain Acetylcholine (emotional changes). this is the main basis for current pharmacotherapy
  3. entorhinal cortex (memory changes)
  4. hippocampus (memory changes)

synapse loss occurs first, then neurons die

44
Q

when do changes begin in an AD brain before symptoms appear

A

10 - 20 years

45
Q

what are the symptoms that appear in the stage 1 of AD

A
  • deficit in recent memory
  • Intellectual deficits confirmed by neuropsychological testing
  • Some awareness of their symptoms, so the person may become anxious, depressed and may be in denial

-No distinguishing features on physical examination

46
Q

In stage 2 of AD (moderate) where are the histopathology signs of AD noticed

A

> TAU and Beta Amyloid proteins spreads through the brain

> the cerebral cortex begins to shrink as more neurons die

47
Q

what are the symptoms that appear in the stage 2 of AD

A

> significant memory loss : forgets close family members, well known routes / places

> personality and behavioural changes (self neglect)

> disorientation in time and space

> inability to undertake simple tasks such as dressing

> reduced range of thinking (intellectual deficits

> language problems

48
Q

In stage 3 of AD (severe) are the histopathology signs of AD noticed

A

> extreme shrinkage of the brain
spread of TAU and BA proteins across the brain

49
Q

what are the symptoms that appear in the stage 3 of AD

A

> Dysphasia with disordered and fragmented
speech
Aggression, restlessness and wandering
Hallucinations and delusions
urinary Incontinence: loss of bladder control
Immobility, rigidity and recurrent falls
General physical deterioration
patient are completely dependent on others on care

50
Q

what is usually the cause of death in stage 3 AD

A

> aspiration pneumonia
other inf ections

51
Q

jerhow long is death from time of clinical diagnosis to death

A

5 - 10 years

INTERGRATED STUDIES IN MENTAL HEALTH (16 decks)

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