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Aging brains and waning clocks on the process of habituation

Impact Journals, LLC
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  • Biology


dSir2 and Dmp53 interact to mediate aspects of CR-dependent life span extension in D Cyclical patterns of activity that occur every twenty- four hours are referred to as circadian oscillations. Most organisms experience circadian oscillations of some kind and human biology sustains numerous circadian oscillations that support complex physiological functions. As we age, the circadian clock begins to break down. For example, the molecular rhythmicity in expression or activity of some proteins dampens and our sleep/wake cycles become disrupted. This waning clock may have numerous consequences on our cognitive processes including learning and memory. That the circadian clock influences learning and memory has been demonstrated repeatedly, however, how individual proteins that comprise the clock machinery contribute to learning and memory is not clear [1]. In the May issue of Aging, Kondratova et al. use mice genetically altered in the Clock, Bmal1, and the Cryptochrome (Cry1 and Cry2) genes to address what properties these circadian clock components impart to these cognitive processes [2]. While the brain assists in synchronization of peripheral clocks, to keep accurate time in the brain as well as the periphery, the circadian clock relies on a central transcriptional and translational feedback loop [3]. In brief, the transcription factors Clock and Bmal1 heterodimerize and activate target gene promoters via E boxes, short motifs generally found in the promoters of many oscillating genes. Two of these target genes include the Per and Cry genes, which dimerize and interact with Clock and Bmal1, to inhibit subsequent Clock:Bmal1-mediated gene transcription. While these proteins are expressed in most tissues of the body, including the hippocampus, how they participate in normal hippocampal function or neuronal plasticity is Commentary

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