Affiliations: [a] Department of Pre-Clinical Sciences, University of the West Indies, St. Augustine Campus, Trinidad & Tobago | [b] Institute of Biomedical & Life Sciences, University of Glasgow, Glasgow, Scotland G12 8QQ, UK
Correspondence:
[*]
Corresponding author: Dr. Jonas I. Addae, Department of Pre-Clinical Sciences, Faculty of Medical Sciences, University of the West Indies, St. Augustine, Trinidad & Tobago. Tel.: +1 1 868 645 2640; Fax: +1 1 868 645 3615; E-mail: addae@carib-link.net.
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 (Aβ) 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. Aβ can mediate neurodegeneration by a complex interaction of neurodegenerative processes that involve increasing extracellular concentration of glutamate, increasing intracellular Ca+2 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 Ca+2 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.
