Flashcards in Alzheimers Deck (43):
most epileptic part of the human brain
HM characteristics, conclusion?
LT memory was impaired, but other cognitive functions were intact; function of LT memory is separate from other cognitive functions
bundle of white matter fibers leaving the hippocampus twd the thalamus/BG/forebrain
lesion in this structure causes?
lesion --> anterograde amnesia (cannot provide ACh to hippocampus)
another structure crucial to memory formation?
medial temporal lobes
associative memory: hearing a sound and assoc w a person and his life story
not assoc w/hippocampus - don't need to remember contextual features
declarative (explicit) memory
nondeclarative (implicit) memory
medial temporal dependent (event learning; recall/recognition)
common complication of dural atrophy
subdural hematoma (easily torn)
EC deposition of fibrillar amyloid-B (inflammation, cytokines, complement etc)
degeneration of neurons via?
phosphorylation of tau protein leads to aggregation and degeneration
found in vessels and leads to breakage
role of microglia
activated and phagocytose debris
AB generation leads to adverse effects; defect in the gamma secretase --> breaks down precursor amyloid in abnormal way generating B-Amyloid --> oxidation, aggregation, inflammation, tau hyperphosphrylation (and microtubules) --> plaques and tangles --> cell death, NT deficit --> cognitive and behavioral changes
definition of dementia (MND): multiple realms
decreased problem-solving, abstraction and other exec fxns
end-stage includes deficits in them all
most common cause of dementia?
the older you are, the more common the cause of dementia is alzheimers
core issue of alzheimers
as progresses, further into disease further back memory recall problems become
visuospatial problems due to
can't groom, take meds, feed oneself
common mut in alzheimers
apo-e4 (double risk)
downs: have an extra copy of the amyloid precursor protein gene so deposit more amyloid since birth
increase in which enzyme in alzheimers?
sudden onset of problems w/attention and arousal
central symptom of alzheimers
5 A's of alzheimers
Aphasia, apraxia, agnosia, executive fxn (abstract reasoning, activities of daily living)
conscious, recollective memory
past experiences influence present performance in absence of specific memory
declarative (not non declarative) memory impaired in what kind of amnesia?
type of declarative LTM that includes where/who with/what time etc --> context/source
type of declLTM that contains factual info but not assoc w specific event
bilateral medial temporal lobe (hippocampus)
language remained normal, IQ increased
role of hippocampus
encoding as well as retrieval
brain atrophy most severe where?
accumulations of paired helical filaments in neuronal cytoplasm; birefringent under polarized light and visualized using silver stain
genetics of alzheimers
which two chromosomes?
which two genes?
which two NT's are decreased?
chromosome 14: presenilin-1
chromosome 1: presenilin-2
apoE-e4 --> higher risk and earlier onset
apoE-e2 is protective
ACh and somatostatin
single most powerful risk factor for dementia?
other risk factors?
age --> 45% over 95y have it
genetics (apoE4, family hx of alz, hx of TBI, dearth of education, late-life depression, CV risk fx
most common cause of dementia?
core sx of dementia?
amnesia (2-3y prior to dementia dx)
STM first, then LTM
aphasia, visuospatial, exec dysfxn
criteria for MND due to alzheimers
A. Criteria met for major/mild NCD
B. Insidious onset/gradual progression of impairment in 1+ cognitive domains
C. Criteria met for alzheimers (probable if either of the following, otherwise "possible"):
1. causative genetic mutation
2. all 3 of the following: a) decline in memory/learning and 1+ other domain; b) steadily prog/gradual decline in cognition w/o extended plateaus; c) no evidence of mixed etiology
most pts btwn 75-85y
6-12y from dx to death
donepezil, galantamine, rivastigmine, memantine not effective for?
meds used in dementia
which med assoc w incr mortality in elders w/dementia?
SSRI's and atypical antipsychotics
strokes here lead to problems with attention
strokes here lead to apathy, disinhibition
sudden change in cognitive fxn indicates?
the onset of cognitive sx at least 1y after onset of motor sx, impairment due to Lewy bodies
1) fluctuating sx, 2) visual hallucinations, 3) cognitive impairment, 4) less severe parkinsonian sx than in parkinsons
levy bodies found where?
parkinson's disease dementia
presence of tau inclusion bodies on histo
lobar degeneration of frontal/temporal lobe
when do you know dx of FTD?
course of FTD? death when?
when tx (antidepr/mood stabz) not effective
more rapid than other dementias
death w/in 5y of dx
other causes of dementia
wernicke-korsakoff syndrowm (alcohol dementia)