| pubmed-article:11193794 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11193794 | lifeskim:mentions | umls-concept:C0002395 | lld:lifeskim |
| pubmed-article:11193794 | lifeskim:mentions | umls-concept:C0228174 | lld:lifeskim |
| pubmed-article:11193794 | lifeskim:mentions | umls-concept:C0596402 | lld:lifeskim |
| pubmed-article:11193794 | lifeskim:mentions | umls-concept:C0078939 | lld:lifeskim |
| pubmed-article:11193794 | lifeskim:mentions | umls-concept:C1314792 | lld:lifeskim |
| pubmed-article:11193794 | lifeskim:mentions | umls-concept:C1880156 | lld:lifeskim |
| pubmed-article:11193794 | lifeskim:mentions | umls-concept:C0871935 | lld:lifeskim |
| pubmed-article:11193794 | lifeskim:mentions | umls-concept:C1512571 | lld:lifeskim |
| pubmed-article:11193794 | pubmed:dateCreated | 2001-1-18 | lld:pubmed |
| pubmed-article:11193794 | 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. | lld:pubmed |
| pubmed-article:11193794 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11193794 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11193794 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11193794 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11193794 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11193794 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11193794 | pubmed:issn | 0077-8923 | lld:pubmed |
| pubmed-article:11193794 | pubmed:author | pubmed-author:SelkoeD JDJ | lld:pubmed |
| pubmed-article:11193794 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11193794 | pubmed:volume | 924 | lld:pubmed |
| pubmed-article:11193794 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11193794 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11193794 | pubmed:pagination | 17-25 | lld:pubmed |
| pubmed-article:11193794 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:11193794 | pubmed:meshHeading | pubmed-meshheading:11193794... | lld:pubmed |
| pubmed-article:11193794 | pubmed:meshHeading | pubmed-meshheading:11193794... | lld:pubmed |
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| pubmed-article:11193794 | pubmed:meshHeading | pubmed-meshheading:11193794... | lld:pubmed |
| pubmed-article:11193794 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:11193794 | 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. | lld:pubmed |
| pubmed-article:11193794 | 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 | lld:pubmed |
| pubmed-article:11193794 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11193794 | pubmed:publicationType | Review | lld:pubmed |
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