Journal
NEUROBIOLOGY OF AGING
Volume 30, Issue 7, Pages 1125-1134Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2007.10.001
Keywords
Cognitively impaired not demented; MMSE; Dementia; Compensatory response; Clinico-pathology correlation; Growth-associated protein-43 (GAP-43); Oldest-old; Postsynaptic density (PSD); Synaptophysin (SYN)
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Funding
- Intramural NIH HHS [Z01 AG000658] Funding Source: Medline
- NIA NIH HHS [R01AG21055, R01 AG021055, P50 AG000658, P50 AG16573, P50 AG016573] Funding Source: Medline
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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.
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