The Cholinergic Hypothesis Of Ad And Current Pharmacotherapies

binds to cholinergic autoreceptors on their cell surface. The precise mechanisms for how this might lead to neuron loss or derangement is actively under investigation. Possibilities include direct effects of Ap on the receptors themselves, which are ligand-gated ion channels (74), or elevated intracellular levels of Ap in cholinergic neurons resulting from nicotinic receptor-mediated endocytosis (90, 91).

BOX 2 (A) Immunohistochemical detection of a7 nicotinic ACh Receptor (a7nAChR) in neuritic plaques of AD hippocampus. (a) Tissues were stained with a modified Bielschowsky silver stain technique. Arrowheads indicate areas of neuritic plaques. Tissues were then stained with the appropriate antibodies to either amyloid beta peptide or a7nAChR. (b) Arrowheads indicate neurofibrillary tangles. (c) Presence of AP1-42 (arrowheads) in a dense core plaque. (d) Presence of AP1-42 (arrowheads) in neurons. (e) Presence of a7nAChR (arrowheads) in a neuritic plaque. (f) Presence of a7nAChR (arrowheads) in neurons. (g) Lack of a4nAChR immunoreactivity in a plaque (arrowhead) in a section stained with an alpha4 nicotinic receptor-selective antibody. (h) Lack of N-methyl-D-aspartate R1 glutamate receptor immunoreactivity in a plaque (arrowhead) stained with an NMDAR antibody. Magnification: (a) x 20; (b-h) x 40. All 12 AD brain samples showed identical results, and representative data from two cases of sporadic AD are shown.

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