| pubmed-article:9572056 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9572056 | lifeskim:mentions | umls-concept:C0002395 | lld:lifeskim |
| pubmed-article:9572056 | lifeskim:mentions | umls-concept:C0699748 | lld:lifeskim |
| pubmed-article:9572056 | lifeskim:mentions | umls-concept:C1521991 | lld:lifeskim |
| pubmed-article:9572056 | lifeskim:mentions | umls-concept:C1832428 | lld:lifeskim |
| pubmed-article:9572056 | lifeskim:mentions | umls-concept:C0205422 | lld:lifeskim |
| pubmed-article:9572056 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:9572056 | pubmed:dateCreated | 1998-7-6 | lld:pubmed |
| pubmed-article:9572056 | pubmed:abstractText | Our understanding of the pathogenesis of Alzheimer's disease (AD) comes primarily from the study of rare inherited forms of the disease. Mutations that cause familial AD appear to act by a common mechanism: that of increasing production of A beta 42/43, one of the family of A beta peptides deposited in senile plaques. However, increased A beta 42/43 production has not been demonstrated to occur in most cases of sporadic AD, suggesting that genetic and environmental factors acting at other stages of the disease process can modify the risk for disease. Such factors most likely include those affecting A beta aggregation or clearance, the inflammatory response, cerebrovascular disease, or susceptibility of neurons to injury. Identifying these factors will lead to a better understanding of the etiology of the disease and provide additional targets for therapeutic intervention. | lld:pubmed |
| pubmed-article:9572056 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9572056 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9572056 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9572056 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:9572056 | pubmed:issn | 1357-4310 | lld:pubmed |
| pubmed-article:9572056 | pubmed:author | pubmed-author:GEEJ BJB | lld:pubmed |
| pubmed-article:9572056 | pubmed:author | pubmed-author:GreenY NYN | lld:pubmed |
| pubmed-article:9572056 | pubmed:author | pubmed-author:AshallFF | lld:pubmed |
| pubmed-article:9572056 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9572056 | pubmed:volume | 4 | lld:pubmed |
| pubmed-article:9572056 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9572056 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9572056 | pubmed:pagination | 151-7 | lld:pubmed |
| pubmed-article:9572056 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:9572056 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9572056 | pubmed:articleTitle | Molecular pathogenesis of sporadic and familial forms of Alzheimer's disease. | lld:pubmed |
| pubmed-article:9572056 | pubmed:affiliation | Department of Psychiatry, Washington University School of Medicine, St Louis, MO 63110, USA. goate@icarus.wustl.edu | lld:pubmed |
| pubmed-article:9572056 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9572056 | pubmed:publicationType | Review | lld:pubmed |
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