New research suggests that accumulation of amyloid-â peptides in cerebral blood vessels, as opposed to the brain itself, may be a more important pathological mediator of Alzheimers disease. Two independent yet related articles describe such findings in the August issue of The American Journal of Pathology. Both articles are highlighted on the Journals cover.
Alzheimers disease, the most common form of progressive dementia, affects an estimated 4.5 million Americans according to the Alzheimers Association. Amyloid-â (Aâ) deposition is a hallmark of Alzheimers disease and other cerebral amyloid angiopathies. However, exactly how Aâ accumulates and causes damage is not fully understood.
In the first article, "Cerebral microvascular Aâ deposition induces vascular degeneration and neuroinflammation in transgenic mice expressing human vasculotropic mutant AâPP," Miao et al. describe early-onset Aâ deposition in Tg-SwDI mice. These mice express Aâ protein with mutations that are found in human early-onset cerebral amyloid angiopathy, causing specific accumulation of Aâ in cerebral blood vessels.
Audra Cox | EurekAlert!
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