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Research article summary (published 30 Mar 2003):

Neuroprotective role of learning in dementia: a biological explanation.

Full Abstract

Several epidemiological studies have found an association between low educational level (or low cognitively demanding occupations) and dementia. Although other studies have not found evidence to support such an association, there has been a general trend toward a "use it or lose it" concept which attempts to promote a neuroprotective role of intellectual activity against the development of dementia. Formation of amyloid-beta peptide (Abeta) in the brain plays a key role in the development of Alzheimer's disease whilst glutamate has been implicated in the pathophysiology of a number of neurological disorders including Alzheimer's disease and vascular dementia. Abeta can mediate neurodegeneration by a complex interaction of neurodegenerative processes that involve increasing extracellular concentration of glutamate, increasing intracellular Ca2+ concentration, and apoptosis. Long-term potentiation (LTP, a biological correlate of learning and memory) increases the sensitivity of hippocampal neurons to synaptically released glutamate whilst decreasing responses of neurons to bath applied glutamate receptor agonists and to hypoxia/ischemia in vitro. The effects of LTP are likely to involve changes in intracellular Ca2+ concentration. Based on these findings we are proposing that the LTP-induced neuroprotection in vitro may help explain the epidemiological evidence of a possible neuroprotective role of high intellectual activity against dementia.

 

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Author information

Author/s: Addae, Jonas I (JI); Youssef, Farid F (FF); Stone, Trevor W (TW);

Affiliation: Department of Pre-Clinical Sciences, University of the West Indies, St Augustine Campus, Trinidad & Tobago. addae(-atsign-)carib-link.net

Journal and publication information

Publication Type: Journal Article; Review

Journal: Journal of Alzheimer's disease : JAD (J Alzheimers Dis), published in Netherlands. (Language: eng)

Reference: 2003-Apr; vol 5 (issue 2) : pp 91-104

Dates: Created 2003/04/29; Completed 2003/09/16; Revised 2005/11/16;

PMID: 12719627, 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: Amyloid beta-Protein Precursor (0) ; Receptors, Glutamate (0) ; Glutamic Acid (56-86-0) ; Calcium (7440-70-2)

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