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22 Cards in this Set
- Front
- Back
What is Alzheimer's Disease? |
A chronic neurodegenerative that accounts for most cases of dementia. |
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What causes familial AD? |
Dominant mutations in genes |
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What are the genes that cause familial AD? |
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What is Beta amyloid precursor protein implicated in? |
Synapse formation and regulation, neural plasticity and iron export.
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What is B-Amyloid deposition a pathological feature of? |
AD and normal ageing |
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Mutations cluster near parts important for what function? |
Cleavage (cutting up proteins) |
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What is TREM2's role? |
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What are PSEN1 & 2? |
Transmembrane proteins and components of gamma secretase. |
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What does Gamma Secretase do? |
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What is the amyloid hypothesis? |
Extracellular amyloid beta deposits (deposits outside the cell) are the main cause of AD. |
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What is the major genetic risk factor in sporadic AD? |
ApoE4 allele |
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What is the main function of ApoE? |
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How is ApoE4 implicated in sporadic AD? |
It is not good at amyloid beta breakdown causing a build up of the protein, thus linking to the amyloid hypothesis. ApoE4 is BAD NEWS. |
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What is the risk of developing AD with ApoE4? |
1 = 2-3x risk 2 = 12x risk Also linked to early age onset |
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What are the main symptoms of AD? |
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What is the main diagnostic problem with AD? |
Preclinical AD may be mistaken for normal ageing and when symptoms finally become noticeable it becomes clinical AD and too late for treatment. |
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What is the treatment for AD? |
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How do cholinesterase inhibitors work in AD? |
Prevent acetylcholinesterase breaking down acetylcholine and thus increasing nerve connections. |
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How do NMDA receptor antagonists work in AD? |
Blocks excess glutamate production which is secreted from damaged cells which cause further damage to more cells. |
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Why are antipsychotics prescribed to AD patients? |
To deal with aggressive and psychotic symptoms. |
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What supportive measures can be taken for AD patients? |
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What are the cortical abnormalities presented in AD? |
Cortical atrophy - Particularly ventricles and hippocampus |