CHAPTER 19 - ALZHEIMER

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38 Terms

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Alzheimer’s disease

neurodegenerative disease causing dementia

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dementia

progressive decline in cogntiion severe enought to interfere with being able to function independentlu

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what is usuallly the first symtpom of dementia

gradual progressive memory loss

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What do we need to distinguish for the diagnosis of AD and dementia

the clinical syndrome and aetiologic subtype

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give the three diagnostic criteria for dementia

1) signficant cogntive decline in one or more cognitive domains, with concerns from either the individual or an informant

2) cognitive impairment is severe enough to interfere with independence in everyday life

3) cognitive impairmenst don’t occur in the context of a delirium and can’t be explain

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Mild cognitive impairment

ability to function independently is relatively intact

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what can MCI be considered as

prodromal stage of AD, but some don’t have an underlying neurogenerative disease and never develop dementia

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what % of people develop dementia within 5 -10 years after the diagnosis of MCI, and with increases the likelihood

50%
likelihood increases if there is evidence of both cognitive profile that aligns with that of early AD, and a positive biomarker reflecting the AD’S pathophysiological process

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give the three points in diagnostic criteria of MCI

1) modest cognitive decline established by an objective cognitive assessment, and the individual informant

2) no interference with independence in everyday activities

3) cognitive impairment doesn’t occur in the context of a delirium and can’t be explained by another mental disorder

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give the prevalence of young dementia and dementia
- men or women?
-differences between men and women
- how long do you survive after diagnosis

young dementia is underdiagnosed because it’s not easily recognized
About 1 in 5 develops dementia

The risk to develop dementia is higher in women (1/3) than for males (1/7)
There is differences in life expectancy, genetics, biological and socio-economic risks

person survives on average 7-10 years

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Talk about the plagues and tangels in AD

  • also how can we confirm

    • how can we assess different neuropathological features

abnormal accumulation and deposition of extracellular plaques of the amyloid-beta protein (senile plagues) and intracellular tangles of the protein tau (neurfibrillary tangles), which lead to degeneration of nerve cells and atrophy (neurodegeneration)

only possible to confirm AD post-mortem

best to assess with CT, MRI, molecular imaging, and CSF

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what is the amyloid cascade hypothesis

→ also how does accumulation of amyloid-beta plagues lead to dementia?

an abnormal accumulation of the amyloi-dbeta protein is the primary driver of AD

  • peoplel with a mutation in the APP gene have an overproduction of beta-amyloid and all developed AD eventually

  • accumulation of amyloid-beta plagues → propagation of tau pathology → synapse loss → neuronal death → cognitive decline → dementia

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explain the vascular hypothesis

vascular risk factors lead to reduced blood flow and oxygen deficiency in the brain. this leads to stiffening of the arterial wallss and a metaboloic reaction that causes an overproduction of the amyloid-beta protein and neurodegeneration

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what is the clinical course of AD

subtle cognitive changes → increasingly persistent cognitive decline → functional impairment → dementia syndrome

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what occurs in rare cases of AD, and what is iportant to do for this

some patients present other symptoms and have less prominent memory problems, which is why it is important to have an interview with both the informant and patient

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What are the stages of AD

1) MCI

2) mild dementia and moderate dementia

3) severe dementia

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Clinical Dementia Rating Scale

semi-structured interview where cognitve and functional performance is rated in six domains

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what are the six domains rated in the clinical dementia rating

memory, orientation, problem-solving, social activities, home & hobbies, and personal care

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cognitive profile of ad

prominent episodic memory deficits → decline in semantic memory, language, working memory, and executive functions → visuoconstructive and praxis deficits

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give the clinical stages with corresponding global CDR score

1) Amenstic MCI as predementia stage (CDR;0.5)

2) Mild dementia (CDR;1)

3) Moderate dementia (CDR;2)

4) Severe dementia (CDR;3)

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why are biomarkers found through structural neuroimaging used to diagnose AD

to rule out another neurological disorder, and to identify positive signs for th etiological cause of AD.

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what brain changes can we see in AD

typical pattern of grey matter loss: medio temporal lobe → posterior and frontal cortical regions → global cortical atropy

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what is inspected first in the brain when AD is suspected, and how can we assess the atropy.

the structure and volume of the hippocampus are first. The atrophy of the hippocampal areas is assessed witht the Scheltens scale

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How is the MTA score calculated

with a T1-weighted coronal section

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what is the MTA score based on

1) width of choroid fissure

2) width of temporal horn

3) height of the hippocampus

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Explain what EEG and PET can do

EEG: can find the most characteristic abnormality consistent with AD

PET; provides an alternative way to measure functional abnormalities in the brain, by measuring reduction in the cerebral metabolic rate for glucose

→ can help detect abnormalities in temporo-parietal regions in the early stages

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what do the abnormal scans correlate with

with having cerebral amyloid pathology at post-mortal examination

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Why are abnormal scans not used routinely

because they can happen in older peopel without dementia and the amount of amyloid deposition doesn’t stronly correlate with disease severity

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what is aa typical CSF profile for AD

decreased concentraion of amyloid-beta and an increased concentration of tau and p-tau

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what are the pros for CSF profile

cheaper, quicker, and easier

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what are the cons for CSF profile

doesn’t provide informatino about the localization of pathology

CSF biomarkers may have value in increasing the certainty of diagnosis, but the diagnostic value also appears to decrease with age

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atypical variants start in different cortical regions and lead to different cognitive symptoms in the initial stage of the diasse. Which three variants are there?

  1. posterior cortical atropy (PCA)

  2. logopenic vairant primary progressive aphasia (vpPPA)

  3. behavioural variant/dysexecutive function

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explain the posterior cortical atrophy

  • prominent deficits

  • what remains intact

    • where does pattern of neurodegeneration start

prominent deficits in the visuospatial functions, and memory remains relatively intact

pattern of neurodegeneration usually starts in parietal and occipital lobe and then spreads to occipitotemporal lobe

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explain the logopenic variant primary progressive aphasia

  • where initial deficits

  • where later deficits

    • how is atrophy distributed and where

predominant language and communication deficits, and later also language comprehension, executive functions and verbal memory

atrophy is distributed asymmetrical and most in left temporal lobe

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explain the behavioural variant

  • where is the atrophy

behavioural changes and impairments in executive function and social cognition

atrophy is most pronounced in the frontal lobe regions

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which neuropsychiatric symptoms are common for people with dementia

agitation, depression, anxiety, apathy, delusions, sleep impairment, and hallucinations

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prevalence of neuropsychiatric symptoms in MCI stage and dementia stage

13 to 85% in MCI stage and 50 to 98% in dementia stage

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why is a proper diagnosis of neuropsychiatric symptoms important to have

because the symptoms have a negative impact on the quality of life and are assocaited with faster disease progression and increased risk of institutionalization