期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 281, 期 51, 页码 39413-39423出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M608485200
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资金
- NIA NIH HHS [AG20241, AG0212982] Funding Source: Medline
Increasing evidence points to soluble assemblies of aggregating proteins as a major mediator of neuronal and synaptic dysfunction. In Alzheimer disease ( AD), soluble amyloid-beta (A beta) appears to be a key factor in inducing synaptic and cognitive abnormalities. Here we report the novel finding that soluble tau also plays a role in the cognitive decline in the presence of concomitant A beta pathology. We describe improved cognitive function following a reduction in both soluble A beta and tau levels after active or passive immunization in advanced aged 3xTg-AD mice that contain both amyloid plaques and neurofibrillary tangles (NFTs). Notably, reducing soluble A beta alone did not improve the cognitive phenotype in mice with plaques and NFTs. Our results show that A beta immunotherapy reduces soluble tau and ameliorates behavioral deficit in old transgenic mice.
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