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Nicotinic Acetylcholine Receptor Signaling in Neuroprotection
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Accumulation of amyloid β protein (Aβ) in the brain causes cognitive impairment in Alzheimer’s disease (AD). The nature of the relationship between smoking and AD or dementia has been controversial. However, a recent meta-analysis revealed that smoking is a risk factor for AD. With regard to
Myopathy in cattle induced by alkaloid extracts from Thermopsis montanta, Laburnum anagyroides and a Lupinus sp.
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A purified alkaloid preparation containing N-methylcytisine, cytisine, 5,6-dehydrolupanine, thermopsine and anagyrine from Thermopsis montana induced prolonged recumbency and microscopic acute hyaline skeletal myodegeneration with myofibre regeneration in cattle similar in type and severity to that
Amyloid peptide Abeta(1-42) binds selectively and with picomolar affinity to alpha7 nicotinic acetylcholine receptors.
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We have recently reported evidence that a very high affinity interaction between the beta-amyloid peptide Abeta(1-42) and the alpha7 nicotinic acetylcholine receptor (alpha7nAChR) may be a precipitating event in the formation of amyloid plaques in Alzheimer's disease. In the present study, the
Quantitative changes of nicotinic receptors in the hippocampus of dystrophin-deficient mice.
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Lack of dystrophin in Duchenne muscle dystrophy (DMD) and in the mutant mdx mouse results in progressive muscle degeneration, structural changes at the neuromuscular junction, and destabilization of the nicotinic acetylcholine receptors (nAChRs). One-third of DMD patients also present
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