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Biotech / Medical : Neuroscience -- Ignore unavailable to you. Want to Upgrade?

To: Jim Oravetz who wrote (158)	1/8/2001 8:55:09 AM
From: scott_jiminez	Respond to of 278

The critical piece of information would be the sequence of events. It's been known for over 20 years that the cholinergic cells in the Nucleus Basalis (which project to - and thus provide the acetylcholine-mediated neurotransmission to - the hippocampus) degenerate during the course of AD. In fact, the loss of the basalis cells served as the basis of one theory of the disease in the 1980s (see 'The Cholinergic Hypothesis of Alzheimer's Disease' by Peter Davies in Science in ~1984. The same author published an article entitled, 'Challenging the cholinergic hypothesis in Alzheimer disease.' in JAMA last year.). Thus (without having read the NIEHS papers) there appears to be at least two possibilities here: 1. Amyloid has a particular affinity for cholinergic receptors, as the authors imply, thereby leading to disruption of terminal integrity, and the ultimate demise, of the parent cholinergic cells, or 2. the cholinergic cells in the basalis degenerate as part of the AD pathology thereby 'vacating' their postsynaptic fields (read: receptors) and leaving these receptors available for 'sticky' proteins such as amyloid to bind. The distinction between these two scenarios is critical: if amyloid disrupts intact cholinergic receptors then 'blocking' amyloid may have profound effects. If amyloid is binding to ACh receptors previously vacated by the degenerating axons of cholinergic cells, then the amyloid/receptor interaction is more of a tag for a stage of the disease than an opportunity to thwart the progression of the disease.