pubmed-article:20726888 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C0001792 | lld:lifeskim |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C0002395 | lld:lifeskim |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C0026447 | lld:lifeskim |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C0005839 | lld:lifeskim |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C0007776 | lld:lifeskim |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C0206181 | lld:lifeskim |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C0002716 | lld:lifeskim |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C0699748 | lld:lifeskim |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C1711206 | lld:lifeskim |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C1709305 | lld:lifeskim |
pubmed-article:20726888 | lifeskim:mentions | umls-concept:C0702240 | lld:lifeskim |
pubmed-article:20726888 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:20726888 | pubmed:dateCreated | 2010-11-2 | lld:pubmed |
pubmed-article:20726888 | pubmed:abstractText | Alzheimer's disease (AD) is the most common dementia-causing disorder in the elderly; it may be related to multiple risk factors, and is characterized pathologically by cerebral hypometabolism, paravascular ?-amyloid peptide (A?) plaques, neuritic dystrophy, and intra-neuronal aggregation of phosphorylated tau. To explore potential pathogenic links among some of these lesions, we examined ?-secretase-1 (BACE1) alterations relative to A? deposition, neuritic pathology and vascular organization in aged monkey and AD human cerebral cortex. Western blot analyses detected increased levels of BACE1 protein and ?-site-cleavage amyloid precursor protein C-terminal fragments in plaque-bearing human and monkey cortex relative to controls. In immunohistochemistry, locally elevated BACE1 immunoreactivity (IR) occurred in AD but not in control human cortex, with a trend for increased overall density among cases with greater plaque pathology. In double-labeling preparations, BACE1 IR colocalized with immunolabeling for A? but not for phosphorylated tau. In perfusion-fixed monkey cortex, locally increased BACE1 IR co-existed with intra-axonal and extracellular A? IR among virtually all neuritic plaques, ranging from primitive to typical cored forms. This BACE1 labeling localized to swollen/sprouting axon terminals that might co-express one or another neuronal phenotype markers (GABAergic, glutamatergic, cholinergic, or catecholaminergic). Importantly, these BACE1-labeled dystrophic axons resided near to or in direct contact with blood vessels. These findings suggest that plaque formation in AD or normal aged primates relates to a multisystem axonal pathogenesis that occurs in partnership with a potential vascular or metabolic deficit. The data provide a mechanistic explanation for why senile plaques are present preferentially near the cerebral vasculature. | lld:pubmed |
pubmed-article:20726888 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20726888 | pubmed:language | eng | lld:pubmed |
pubmed-article:20726888 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20726888 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:20726888 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20726888 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20726888 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20726888 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20726888 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20726888 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20726888 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20726888 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20726888 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20726888 | pubmed:month | Oct | lld:pubmed |
pubmed-article:20726888 | pubmed:issn | 1460-9568 | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:XiongKunK | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:KordowerJeffr... | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:CaiYanY | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:YanXiao-XinXX | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:StrubleRobert... | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:ZhangXue-MeiX... | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:ChuYapingY | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:CaiHuaibinH | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:CloughRichard... | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:PatryloPeter... | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:LuoXue-GangXG | lld:pubmed |
pubmed-article:20726888 | pubmed:author | pubmed-author:FengJia-ChunJ... | lld:pubmed |
pubmed-article:20726888 | pubmed:copyrightInfo | © 2010 The Authors. European Journal of Neuroscience © 2010 Federation of European Neuroscience Societies and Blackwell Publishing Ltd. | lld:pubmed |
pubmed-article:20726888 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20726888 | pubmed:volume | 32 | lld:pubmed |
pubmed-article:20726888 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20726888 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20726888 | pubmed:pagination | 1223-38 | lld:pubmed |
pubmed-article:20726888 | pubmed:dateRevised | 2011-10-3 | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:meshHeading | pubmed-meshheading:20726888... | lld:pubmed |
pubmed-article:20726888 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20726888 | pubmed:articleTitle | ?-Secretase-1 elevation in aged monkey and Alzheimer's disease human cerebral cortex occurs around the vasculature in partnership with multisystem axon terminal pathogenesis and ?-amyloid accumulation. | lld:pubmed |
pubmed-article:20726888 | pubmed:affiliation | Department of Anatomy and Neurobiology, Central South University Xiangya Medical School, Changsha, Hunan, China. | lld:pubmed |
pubmed-article:20726888 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20726888 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:20726888 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
pubmed-article:20726888 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
entrez-gene:23621 | entrezgene:pubmed | pubmed-article:20726888 | lld:entrezgene |
http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:20726888 | lld:entrezgene |