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9 Cards in this Set
- Front
- Back
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what is AD also known as?
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tauopathy. (neurodegenerative disease associated with tau protein)
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explain how the aggregation of tau protein happens in AD?
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tau becomes abnormally phosphorylated in AD.
it forms intracellular deposits. tangles are formed via the hyper-phosphorylation of tau, these aggregations are known as PHF (paired helical filaments). after cell death PHFs aggregate into extracellular neurofibrillary tangles. NFTs. |
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what is AD characterised by?
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loss of cholinergic neurones in the basal forebrain nuclei
ChAT, ACh, AChE & choline transport in the cortex and hippocampus all reduce. nAChR reduced (in cortex esp.) there's no evidence for how/why beta amyloid plaques form, but it could be due to a loss of cholinergic neurones. |
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what are the two main therapies for AD atm?
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we currently use AChE inhibitors and memantine (NMDA receptor antagonist.)
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what do AChE inhibitors do?
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enhances cholinergic transmission, which may compensate for the cholinergic deficit
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give an example of an AChE inhibitor?
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TACRINE.
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outline some details of AChE inhibitors? Why aren't they very good?
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they were the first approved treatment. Had to be taken every 6h and could cause side-effects like nausea and hepatotoxicity.
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Name other AChE inhibitors?
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Donezepil, rivastigmine, galantamine.
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name a future target for the treatment of AD?
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beta and gamma secretase. Inhibition of these could stop neurodegeneration.
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