Term
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Definition
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Term
| *AD will increase in % as size of elderly pop increases |
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Definition
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Term
| most frequnet cause of death with AD |
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Definition
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Term
AD is the major dementia- what % is it?
_ leading cause of death |
|
Definition
50%
4th (its also only human disease) |
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Term
primary risk factor forAD
what % is genetic? |
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Definition
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Term
| sporadic AD or familial is more ocmmon |
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Definition
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Term
at what age is alzheimers early onset"?
what class is most common here |
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Definition
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Term
when is alzhimer late onset
which class is more common |
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Definition
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Term
AD more common in men or women?
why |
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Definition
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Term
| what increases risk of AD-3 |
|
Definition
hypercholesterol
obesity
trisomony 21 |
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Term
| what can reduce risk of AD? -2 |
|
Definition
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Term
| *no env factors have been proven to cause AD |
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Definition
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|
Term
familial AD has what mutations assoc-
(in autosomal dominant) |
|
Definition
presenilin 1 and presenilin 2 (beta amyloid produciton)
amyloid precursor rpotein |
|
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Term
| mutations for AD are not causual, can have them and not have the disease* |
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Definition
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Term
| which is the best studied gene for AD |
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Definition
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Term
| Apolipio E4 allele does what-2 |
|
Definition
decrease age onset
increase seveirity
(more % is found in older age) |
|
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Term
| * all with trisomy 21 will get AD, with amyloid plaques 3 decades earlier than other ppl |
|
Definition
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Term
|
Definition
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|
Term
what imaging can dx AD?
what does it look for?
what cant it do? |
|
Definition
amyvid
vizamyl (come from Congo REd)
plagues
tx response or predict future AD |
|
|
Term
| where do amyloid plaques form in AD-2 |
|
Definition
|
|
Term
| what are the main amyloid beta plaques made of? |
|
Definition
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|
Term
| whcih type of plaques have a core amyloid with a ahlp surrounding? |
|
Definition
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|
Term
| what plaques dont have halo? |
|
Definition
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|
Term
| which plaques appear with aging and whcih with AD? |
|
Definition
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|
Term
| neurofibrillary tangles are aggreations of? |
|
Definition
| tau (paired helical filaments) PHF |
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Term
| * in AD there is neuron death and brain atrophy! |
|
Definition
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Term
| the selective vulneraility in AD is that the neurons in _ layers of the assoicative cortices are lost |
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Definition
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Term
| which regions of the brain are spared until later in the disease |
|
Definition
| primary motor and sensory |
|
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Term
| which regions of the brain are the frist to show nuerofibril tangles?-2 |
|
Definition
enotohinol
hippocampal of temporal cortex )this stores memories) |
|
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Term
| the loss of cholinergic neurons in the nucelus basalis of meynert and septum normally inmervate what? -2 |
|
Definition
hippocampus
cerebral cortex |
|
|
Term
| septal neurons promote learnign and meomry how? |
|
Definition
| rlease ACH-> synaptic plasitcity |
|
|
Term
| *hippocampus and septal neurons are among first neurons to be lost in AD |
|
Definition
|
|
Term
| amyloid paques appear first where |
|
Definition
| ventral of frontal and temporlal cortex |
|
|
Term
amyloid appears later where?
examples of this region:-4 |
|
Definition
subcortical
hypothalmus, thalamus, striatium, brainstem |
|
|
Term
| neurofibrillary tangles first appear? |
|
Definition
| entorhinal->hippocampus->associaiton |
|
|
Term
| neurofibrillary has progressed to where when AD can be recognized in pts |
|
Definition
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|
Term
| *AD begins with plaques and neurotangles in cortical and in late stage the subcortical regions |
|
Definition
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|
Term
cardinal feature of AD is-
the reason they seek medical attneiton is- |
|
Definition
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|
Term
| is degree of dementia correlated to number of senile plaques? |
|
Definition
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|
Term
| dementia is best correlate with what? |
|
Definition
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|
Term
| whic occurs first metabolic or cognitive symtpoms? |
|
Definition
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|
Term
| as cognitive function decreases in AD, what also decreaases? |
|
Definition
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|
Term
| lesion of hippocampus will result in? |
|
Definition
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|
Term
| cholinergic cells in the _ facilitate neuron plasticity |
|
Definition
|
|
Term
the entorhinal cortex coneects the hippocampus to-
destruction of this interferes with? |
|
Definition
neocortex
memroy consolidaiton |
|
|
Term
| due to entorhinal and hippocampus are frist reginos to be hit in AD, what are the first symtpoms? |
|
Definition
|
|
Term
| the non amyloidgenic process of the amyloid precursor protein is |
|
Definition
|
|
Term
| what proteases of the amyloi precurose rpotein make fibrils to become plaques |
|
Definition
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|
Term
| * BA4 makes glutamergic neurons more senstive to Ca overload and oxidative stress |
|
Definition
|
|
Term
| glu antagonists (dihydroperidines) can actually be helpful to block neurotoxic effects of BA4 |
|
Definition
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|
Term
*mutaitons in APP cause more BA4 (neurotoxic) or a longer Ba49 which is amlyoidgenic
*mutations in presneilins do this too |
|
Definition
|
|
Term
| ApoE bind BA4 to prvent aggregation. E4 does this less than E3 |
|
Definition
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|
Term
| APP gene is located where? |
|
Definition
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|
Term
| APP HAS GREATER EXPERSSION WHERE? |
|
Definition
| hippocampus and associaiton cortex |
|
|
Term
| anti-infalmmatories prevent reactive O2 species |
|
Definition
|
|
Term
| estrogen is a trophic factors for the brain to counteract apoptpsis and antioxdiant |
|
Definition
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