Cognitive impairment places a severe burden upon both the sufferers and their carers. While approximately 5-10% of patients displaying cognitive impairment possess a genetic predisposition, such as a Flemish or Swedish mutation in the amyloid pre-cursor protein, the majority of patients do not possess such an obvious cause of their malady. The causes of age-dependent cognitive decline in the general population are likely to extremely diverse and therefore multifactorial. However there is one phenomenon that is generally expressed in the population, cognitive performance in tasks, that appears to be positively correlated to a prophylactic action against age-dependent neurodegeneration. This underlies the anecdotal adage of the use it or lose it phenomenon. Hence in this study we are attempting to understand not only the natural basis for cognitive capacity but also hopefully elucidate signaling mechanisms that are linked to this capacity that possess an intrinsic neuroprotective action. We are already nearing the completion of the first phase of this study in which we have used a large genetically identical murine pool of both male and female animals. We are in the process of generating a semi-quantitative relationship between protein expression in the cortex and hippocampus of these animals and their maze solving capacity. We feel that the data derived from this study will illuminate the field of cognition and provide a novel insight into the molecular basis of individual intellectual variation.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Investigator-Initiated Intramural Research Projects (ZIA)
Project #
1ZIAAG000319-05
Application #
8552366
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
5
Fiscal Year
2012
Total Cost
$243,878
Indirect Cost
Name
National Institute on Aging
Department
Type
DUNS #
City
State
Country
Zip Code
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Jasien, Joan; Daimon, Caitlin M; Maudsley, Stuart et al. (2012) Aging and bone health in individuals with developmental disabilities. Int J Endocrinol 2012:469235

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