Source:http://linkedlifedata.com/resource/pubmed/id/11193794
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
2001-1-18
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pubmed:abstractText |
A central challenge of research on Alzheimer's disease (AD) is to assemble the enormous body of scientific observations about the disorder, some of them seemingly in conflict with others, into a coherent and credible mechanism of pathogenesis. In this article, I attempt to synthesize the disparate findings on AD into a unified sequence that essentially begins with alterations in the production or clearance of the amyloid beta-protein (A beta). Mounting evidence from many laboratories supports an A beta accumulation in limbic and association cortices as the fundamental initiator of the disease, with attendant therapeutic implications.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0077-8923
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
924
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
17-25
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11193794-Alzheimer Disease,
pubmed-meshheading:11193794-Amyloid beta-Peptides,
pubmed-meshheading:11193794-Brain,
pubmed-meshheading:11193794-Cytotoxins,
pubmed-meshheading:11193794-Humans,
pubmed-meshheading:11193794-Neurofibrillary Tangles,
pubmed-meshheading:11193794-Plaque, Amyloid
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pubmed:year |
2000
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pubmed:articleTitle |
Toward a comprehensive theory for Alzheimer's disease. Hypothesis: Alzheimer's disease is caused by the cerebral accumulation and cytotoxicity of amyloid beta-protein.
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pubmed:affiliation |
Department of Neurology, Harvard Medical School, and Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. boucher@cnd.bwh.harvard.edu
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pubmed:publicationType |
Journal Article,
Review
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