Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8680072 | Alzheimer's & Dementia | 2017 | 8 Pages |
Abstract
People with DS and trisomy 21 produce a large amount of Aβ. If Alzheimer's pathology occurred in DS without microvascular loss or endothelial impairment, a direct neurotoxic Aβ mechanism would be supported and microvascular impairment rejected. The observation of microvascular impairment in DS with Alzheimer's disease changes fails to reject the microvascular hypothesis and provides some support for this potential mechanism of injury.
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Authors
David A. Drachman, Thomas W. Smith, Bassam Alkamachi, Kevin Kane,