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Research article summary (published 30 May 2002):

Synapse loss is greater in presenile than senile onset Alzheimer disease: implications for the cognitive reserve hypothesis.

Full Abstract

In the past, 'Alzheimer disease' (AD) referred to pathologic AD with clinical onset of dementia in the presenium, while 'senile dementia of the Alzheimer type' (SDAT) referred to senile onset AD. Because AD appears clinically homogeneous regardless of age of onset, the two subtypes in more recent years have not been distinguished. Pathologic differences have been noted, but synapse loss has not previously been compared between the two groups. Hypothesizing that synapse loss would be greater in presenile onset than senile onset AD, we compared synapse loss, as well as Alzheimer pathology in presenile and senile onset AD, using an ELISA method to quantify synaptophysin. Synaptophysin was significantly lower in presenile than senile AD in right frontal and bilateral parietal lobes. Neuritic plaque counts were significantly higher in presenile than senile AD in bilateral frontal and parietal lobes. Semi-quantitative evaluation of neurofibrillary tangles revealed significantly more tangles in bilateral frontal and parietal lobes in presenile than senile AD. Brain weight was significantly lower in presenile than senile AD. The differences in synapse loss and Alzheimer-type pathology in presenile and senile onset AD support the hypothesis that 'cognitive reserve' protects the human brain from neurodegenerative disease.

 

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Author information

Author/s: Bigio, Eileen H (EH); Hynan, L S (LS); Sontag, E (E); Satumtira, S (S); White, C L (CL);

Affiliation: Department of Pathology, Northwestern University Medical School, Chicago, Illinois 60611, USA. e-bigio@northwestern.edu

Grants: AG12300 (Agency:United States NIA) ; AG18883 (Agency:United States NIA)

Journal and publication information

Publication Type: Journal Article; Research Support, U.S. Gov't, P.H.S.

Journal: Neuropathology and applied neurobiology (Neuropathol Appl Neurobiol), published in England. (Language: eng)

Reference: 2002-Jun; vol 28 (issue 3) : pp 218-27

Dates: Created 2002/06/12; Completed 2002/08/02; Revised 2007/11/14;

PMID: 12060346, status: MEDLINE (last retrieval date: 11/6/2008)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Associated Chemicals: Synaptophysin (0)

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