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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
27
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pubmed:dateCreated |
2011-7-7
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pubmed:abstractText |
Abnormally accumulated ?-synuclein (?-syn) is a pathological hallmark of Lewy body-related disorders such as Parkinson's disease (PD) and dementia with Lewy body disease (DLB). However, it is not well understood whether and how abnormal accumulation of ?-syn leads to cognitive impairment or dementia in PD and DLB. Furthermore, it is not known whether targeted removal of ?-syn pathology can reverse cognitive decline. Here, we found that the distribution of ?-syn pathology in an inducible ?-syn transgenic mouse model recapitulates that in human DLB. Abnormal accumulation of ?-syn in the limbic system, particularly in the hippocampus, correlated with memory impairment and led to structural synaptic deficits. Furthermore, when ?-syn expression was suppressed, we observed partial clearing of pre-existing ?-syn pathology and reversal of structural synaptic defects, resulting in an improvement in memory function.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1529-2401
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
6
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
10076-87
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pubmed:dateRevised |
2011-9-21
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pubmed:meshHeading |
pubmed-meshheading:21734300-Acoustic Stimulation,
pubmed-meshheading:21734300-Age Factors,
pubmed-meshheading:21734300-Analysis of Variance,
pubmed-meshheading:21734300-Animals,
pubmed-meshheading:21734300-Animals, Newborn,
pubmed-meshheading:21734300-Brain,
pubmed-meshheading:21734300-Calcium-Calmodulin-Dependent Protein Kinase Type 2,
pubmed-meshheading:21734300-Conditioning, Classical,
pubmed-meshheading:21734300-Cues,
pubmed-meshheading:21734300-Disease Models, Animal,
pubmed-meshheading:21734300-Disease Progression,
pubmed-meshheading:21734300-Embryo, Mammalian,
pubmed-meshheading:21734300-Fear,
pubmed-meshheading:21734300-Female,
pubmed-meshheading:21734300-Gene Expression Regulation,
pubmed-meshheading:21734300-Glial Fibrillary Acidic Protein,
pubmed-meshheading:21734300-Gliosis,
pubmed-meshheading:21734300-Humans,
pubmed-meshheading:21734300-Indoles,
pubmed-meshheading:21734300-Lewy Body Disease,
pubmed-meshheading:21734300-Male,
pubmed-meshheading:21734300-Memory Disorders,
pubmed-meshheading:21734300-Mice,
pubmed-meshheading:21734300-Mice, Inbred C57BL,
pubmed-meshheading:21734300-Mice, Transgenic,
pubmed-meshheading:21734300-Mutation,
pubmed-meshheading:21734300-Nerve Degeneration,
pubmed-meshheading:21734300-Nerve Tissue Proteins,
pubmed-meshheading:21734300-Serine,
pubmed-meshheading:21734300-Synapses,
pubmed-meshheading:21734300-alpha-Synuclein
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pubmed:year |
2011
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pubmed:articleTitle |
?-Syn suppression reverses synaptic and memory defects in a mouse model of dementia with Lewy bodies.
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pubmed:affiliation |
Department of Pathology and Laboratory Medicine, Institute on Aging and Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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