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 #
1ZIAAG000319-02
Application #
7963924
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
2
Fiscal Year
2009
Total Cost
$220,109
Indirect Cost
Name
National Institute on Aging
Department
Type
DUNS #
City
State
Country
Zip Code
Martin, Bronwen; Chadwick, Wayne; Yi, Tie et al. (2012) VENNTURE--a novel Venn diagram investigational tool for multiple pharmacological dataset analysis. PLoS One 7:e36911
Stranahan, Alexis M; Martin, Bronwen; Chadwick, Wayne et al. (2012) Metabolic context regulates distinct hypothalamic transcriptional responses to antiaging interventions. Int J Endocrinol 2012:732975
Park, Sung-Soo; Wu, Wells W; Zhou, Yu et al. (2012) Effective correction of experimental errors in quantitative proteomics using stable isotope labeling by amino acids in cell culture (SILAC). J Proteomics 75:3720-32
Maudsley, Stuart; Chadwick, Wayne (2012) Progressive and unconventional pharmacotherapeutic approaches to Alzheimer's disease therapy. Curr Alzheimer Res 9:1-4
Martin, Bronwen; Chadwick, Wayne; Cong, Wei-na et al. (2012) Euglycemic agent-mediated hypothalamic transcriptomic manipulation in the N171-82Q model of Huntington disease is related to their physiological efficacy. J Biol Chem 287:31766-82
Siddiqui, Sana; Fang, Meng; Ni, Bin et al. (2012) Central role of the EGF receptor in neurometabolic aging. Int J Endocrinol 2012:739428
Chadwick, Wayne; Mitchell, Nicholas; Martin, Bronwen et al. (2012) Therapeutic targeting of the endoplasmic reticulum in Alzheimer's disease. Curr Alzheimer Res 9:110-9
Maudsley, S; Patel, S A; Park, S-S et al. (2012) Functional signaling biases in G protein-coupled receptors: Game Theory and receptor dynamics. Mini Rev Med Chem 12:831-40
Driscoll, Ira; Martin, Bronwen; An, Yang et al. (2012) Plasma BDNF is associated with age-related white matter atrophy but not with cognitive function in older, non-demented adults. PLoS One 7:e35217
Wu, Wells W; Wang, Guanghui; Insel, Paul A et al. (2012) Discovery- and target-based protein quantification using iTRAQ and pulsed Q collision induced dissociation (PQD). J Proteomics 75:2480-7

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