Linked Life Data

15858047

Source:http://linkedlifedata.com/resource/pubmed/id/15858047

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
2005-4-28
pubmed:abstractText
Alzheimer's disease (AD) is a progressive neurodegenerative disorder for which there are few therapeutics that affect the underlying disease mechanism. Recent epidemiological studies, however, suggest that lifestyle changes may slow the onset/progression of AD. Here we have used TgCRND8 mice to examine directly the interaction between exercise and the AD cascade. Five months of voluntary exercise resulted in a decrease in extracellular amyloid-beta (Abeta) plaques in the frontal cortex (38%; p = 0.018), the cortex at the level of the hippocampus (53%; p = 0.0003), and the hippocampus (40%; p = 0.06). This was associated with decreased cortical Abeta1-40 (35%; p = 0.005) and Abeta1-42 (22%; p = 0.04) (ELISA). The mechanism appears to be mediated by a change in the processing of the amyloid precursor protein (APP) after short-term exercise, because 1 month of activity decreased the proteolytic fragments of APP [for alpha-C-terminal fragment (alpha-CTF), 54% and p = 0.04; for beta-CTF, 35% and p = 0.03]. This effect was independent of mRNA/protein changes in neprilysin and insulin-degrading enzyme and, instead, may involve neuronal metabolism changes that are known to affect APP processing and to be regulated by exercise. Long-term exercise also enhanced the rate of learning of TgCRND8 animals in the Morris water maze, with significant (p < 0.02) reductions in escape latencies over the first 3 (of 6) trial days. In support of existing epidemiological studies, this investigation demonstrates that exercise is a simple behavioral intervention sufficient to inhibit the normal progression of AD-like neuropathology in the TgCRND8 mouse model.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
27
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4217-21
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15858047-Alzheimer Disease, pubmed-meshheading:15858047-Amyloid, pubmed-meshheading:15858047-Amyloid Precursor Protein Secretases, pubmed-meshheading:15858047-Amyloid beta-Protein Precursor, pubmed-meshheading:15858047-Analysis of Variance, pubmed-meshheading:15858047-Animals, pubmed-meshheading:15858047-Aspartic Acid Endopeptidases, pubmed-meshheading:15858047-Blotting, Western, pubmed-meshheading:15858047-Brain, pubmed-meshheading:15858047-Disease Models, Animal, pubmed-meshheading:15858047-Endopeptidases, pubmed-meshheading:15858047-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:15858047-Female, pubmed-meshheading:15858047-Immunohistochemistry, pubmed-meshheading:15858047-Male, pubmed-meshheading:15858047-Mice, pubmed-meshheading:15858047-Mice, Transgenic, pubmed-meshheading:15858047-Physical Conditioning, Animal, pubmed-meshheading:15858047-RNA, Messenger, pubmed-meshheading:15858047-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15858047-Time Factors
pubmed:year
2005
pubmed:articleTitle
Voluntary exercise decreases amyloid load in a transgenic model of Alzheimer's disease.
pubmed:affiliation
Institute for Brain Aging and Dementia, University of California, Irvine, Irvine, California 92697-4540, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural