Synaptic proteins, neuropathology and cognitive status in the oldest-old

NEUROBIOLOGY OF AGING

卷:30

Article; Proceedings Paper

Head, Elizabeth^1,2  Corrada, Maria M.^1,2  Kahle-Wrobleski, Kristin¹  Kim, Ronald C.^1,3  Sarsoza, Floyd¹  Goodus, Matthew¹  Kawas, Claudia H.^1,2,4 

[1] Univ Calif Irvine, Inst Brain Aging & Dementia, Irvine, CA 92697 USA

[2] Univ Calif Irvine, Dept Neurol, Irvine, CA 92697 USA

[3] Univ Calif Irvine, Dept Pathol, Irvine, CA 92697 USA

[4] Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA

关键词: Cognitively impaired not demented;    MMSE;    Dementia;    Compensatory response;    Clinico-pathology correlation;    Growth-associated protein-43 (GAP-43);    Oldest-old;    Postsynaptic density (PSD);    Synaptophysin (SYN);   

DOI  :  10.1016/j.neurobiolaging.2007.10.001

来源: Elsevier

【 摘 要 】

An increasing number of individuals in our population are surviving to over 90 years and a subset is at risk for developing dementia. However, senile plaque and neurofibrillary tangle pathology do not consistently differentiate individuals with and without dementia. Synaptic protein loss is a feature of aging and dementia and may dissociate 90+ individuals with and without dementia. Synaptophysin (SYN), postsynaptic density 95 (PSD-95) and growth-associated protein 43 (GAP-43) were studied in the frontal cortex of an autopsy series of 32 prospectively followed individuals (92-105 years) with a range of cognitive function. SYN protein levels were decreased in individuals with dementia and increased in those with clinical signs of cognitive impairment insufficient for a diagnosis of dementia. SYN but neither PSD-95 nor GAP-43 protein levels were significantly correlated with mini-mental status examination (MMSE) scores. Frontal cortex SYN protein levels may protect neuronal function in oldest-old individuals and reflect compensatory responses that may be involved with maintaining cognition. (C) 2007 Elsevier Inc. All rights reserved.

【 授权许可】

Free