Amyloid at the blood vessel wall
Article Abstract:
Data from recent research have corroborated an old view of amyloid plaques, that at their center they have amyloid fibrils extruding from an angiopathic blood vessel. In addition, there is clear evidence that amyloid plaques represent the sites of microhemorrhages in Alzheimer disease. This new view is close to the earlier discredited notion that the disease is caused by hardening of the arteries, however, it is crucial to understand the vascular deposition in amyloid-beta for effective treatment.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2006
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Pinpointing plaques with PIB
Article Abstract:
Researchers have introduced amyloid imaging as a new principle, enabling direct visualization of amyloid plaques in human brain, and using a novel positron emission tomography (PET) tracer called Pittsburgh Compound-B (PIB), marked retention of the molecule was observed in Alzheimer disease patients in areas of the brain known to contain large amounts of amyloid-beta plaques. PIB is a thioflavin-T derivative that has physical properties typical of a useful PET tracer.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2006
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The players on the (gamma)-secretase team
Article Abstract:
Presenilin1 (PS1), APH1, and nicastrin together form a stable complex and after association with PEN-2 and cleavage of presenilin, the complex becomes active (gamma)-secretase, and clips its substrate, amyloid precursor protein-C99 (APP-C99) to generate A(beta) species. The accumulation of A(beta) and neurofibrillary tangles (NFTs) precipitated by the PS1mutation causes the cognitive dysfunction associated with early-onset Alzheimer disease.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2006
User Contributions:
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