Alzheimer's disease: L14 Flashcards
what percentage of all dementias are alzheimer’s disease (AD)
50%
prevalence
- 65-70
- > 80
- 2%
2. 20%
diagnosis of AD
- definitive AD diagnosis only made on pathology (brain biopsy)
- can diagnose dementia of the alzheimer type (DAT) during life
AD
- how it arises
- early onset: 3 genes mutate
- sporadically
- APP, PSEN1 & PSEN2
- all alter production of Aβ peptide (principle component of senile plaques)
- individuals with downs syndrome are what to AD?
- precipitating factors?
- prone to develop -> occurring in 40s
- unknown: Godbolt suggests head injury
- sudden decompensation
clinical features of DAT
- onset
- course
- insidious (gradual)
- slow deterioration
- > death M = 8.5 y after onset
DAT phase 1 symptoms
- failing memory
- muddled inefficiency in activities of daily living (ADLs)
- spatial disorientation
- mood disturbance
DAT phase 2 symptoms
- intellect & personality deteriorate
- focal symptoms appear (speech defects)
- disturbance of posture = increased muscle tone
- delusions/hallucinations
DAT phase 3 symptoms
- terminal stage
- profound apathy
- bed ridden
- lose neurological function
- bodily wasting
Mckhann criteria
1. probable
- deficits 2+ areas of cognition: Amnestic presentation & non amnestic (language, visuospatial)
- worsening of memory/ cog.functions
- no disturbance of consciousness
- 40-90 y/o
- biomarkers (blood profile)
Mckhann criteria
2. possible
- variations in onset, presentation or clinical course
- can be made in the presence of another disorder (not considered the cause of the dementia)
Mckhann criteria
3. definite
- histopathological evidence of AD obtained from biopsy or autopsy
Pathology
- atrophied brain (shrunk)
- degeneration of neurons
- glial cell proliferation
- extensive senile plaques
- extensive neurofibrillary tangles
- > intensity of features correlates with severity of dementia
course of neuropathological changes
- hippocampus/ MTL
- spreads posteriorly to parietal cortex
- spreads to frontal cortex
clinical pattern of cognitive impairment in DAT - amnestic presentation
- initially
1. anterograde
2. retrograde
MTL memory impairment (hippocampal)
- anterograde:
- impaired new learning
- impaired delayed recall
- poor recognition memory - retrograde
- intact for remote memories
- reduced for recent retrograde memories
clinical pattern of cognitive impairment in DAT - amnestic presentation
- Wernicke
- Visuospatial
- Wernicke aphasia (temporal lobe)
- word finding difficulties - topographical disorientation (parietal lobes)
- dyspraxia, agnosia & acalculia
clinical pattern of cognitive impairment in DAT - amnestic presentation
- behaviour
- > must see what for diagnosis of DAT?
- behaviour (frontal lobes)
- apathy + agitation
- > functional impact, day to day interference
Treatment/prevention of AD
- pharmacological
- > what does it offer
- re-balance action of acetylcholine
- > maintain quality of life for longer (QOL)
- no clear evidence that anything prevents AD (e.g. diet, cognitive activity)
AD vs normal ageing
- similarity
- difference
- similar changes occur in both
- cognitive function in DAT is significantly impaired to same age peers
MTL (mild cognitive impairment) does what to chances of developing AD?
raises the likelihood of developing AD
AD progression overview
MTL -> posterior TL -> frontal TL
