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- W2480459626 abstract "Amelioration of cholinergic dysfunction in Alzheimer’s disease remains an important therapeutic goal because of the consequences of cholinergic deficits on higher functions. Current therapeutic strategies have been concentrated on the development of new, less toxic and more efficacious anticholinesterases and also muscarinic agents.1 Improvement of cholinergic transmission is a clinical objective aimed at compensating for deficit in acetylcholine levels in the cerebral cortex resulting from attrition of the cholinergic input from the nucleus basalis magnocellularis of Meynert (nbM). However, cholinergic therapy which is based on enhancing the transmitter levels or on administering drugs acting on postsynaptic sites has so far produced only anecdotal improvement. The limitations of this approach are, in part, due to the late appearance of clinical signs at a time when many cortical neurons and nbM cholinergic projections to cortex are already lost." @default.
- W2480459626 created "2016-08-23" @default.
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- W2480459626 date "1995-01-01" @default.
- W2480459626 modified "2023-09-25" @default.
- W2480459626 title "NGF Rescues Cholinergic Cell Bodies of the Primate Nucleus Basalis of Meynert and Induces Compensatory Synaptic Changes in Cortically-Lesioned Rats" @default.
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- W2480459626 doi "https://doi.org/10.1007/978-1-4757-9145-7_90" @default.
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