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Alzheimer’s disease
neurodegenerative disease causing dementia
dementia
progressive decline in cogntiion severe enought to interfere with being able to function independentlu
what is usuallly the first symtpom of dementia
gradual progressive memory loss
What do we need to distinguish for the diagnosis of AD and dementia
the clinical syndrome and aetiologic subtype
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
Mild cognitive impairment
ability to function independently is relatively intact
what can MCI be considered as
prodromal stage of AD, but some don’t have an underlying neurogenerative disease and never develop dementia
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
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
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
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
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
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
what is the clinical course of AD
subtle cognitive changes → increasingly persistent cognitive decline → functional impairment → dementia syndrome
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
What are the stages of AD
1) MCI
2) mild dementia and moderate dementia
3) severe dementia
Clinical Dementia Rating Scale
semi-structured interview where cognitve and functional performance is rated in six domains
what are the six domains rated in the clinical dementia rating
memory, orientation, problem-solving, social activities, home & hobbies, and personal care
cognitive profile of ad
prominent episodic memory deficits → decline in semantic memory, language, working memory, and executive functions → visuoconstructive and praxis deficits
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)
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.
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
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
How is the MTA score calculated
with a T1-weighted coronal section
what is the MTA score based on
1) width of choroid fissure
2) width of temporal horn
3) height of the hippocampus
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
what do the abnormal scans correlate with
with having cerebral amyloid pathology at post-mortal examination
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
what is aa typical CSF profile for AD
decreased concentraion of amyloid-beta and an increased concentration of tau and p-tau
what are the pros for CSF profile
cheaper, quicker, and easier
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
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?
posterior cortical atropy (PCA)
logopenic vairant primary progressive aphasia (vpPPA)
behavioural variant/dysexecutive function
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
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
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
which neuropsychiatric symptoms are common for people with dementia
agitation, depression, anxiety, apathy, delusions, sleep impairment, and hallucinations
prevalence of neuropsychiatric symptoms in MCI stage and dementia stage
13 to 85% in MCI stage and 50 to 98% in dementia stage
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