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Neuroplasticity - Plasticity, Memory, And Aging

age clinical synaptic age ltp learning

As humans age, an impairment of memory occurs that is not associated with neurological damage or disease. The age of onset for this decline varies, but it is clear that this is a selective deficit and not a generalized decrease in cognitive skills. Moreover, the deficit is also apparent in animal models of aging and is manifest as a greater number of trials required to memorize a task and a decrease in memory retention that begins approximately twenty-four hours post-training. Interestingly, LTP also changes with age, typically requiring a more robust stimulus to induce and yielding a synaptic potentiation that decays more rapidly. Since aging animals and humans both maintain the ability to store memory, the fundamental mechanisms that underlie information storage may remain essentially intact. The deficit may not be a lack of ability, but rather a decline in the efficiency of storage—or an inability to maintain the neural plasticity induced during learning. Since the formation of memory is dependent on new protein synthesis, one way to address the decreased stability of memory is to identify proteins made during learning. Consistent with this, synaptic plasticity has at least two temporally distinct components: transient changes that do not require new protein synthesis, and enduring modifications (e.g., LTP and LTD) that require the production of new proteins. Identification of newly formed proteins, their site of action, and the molecular basis for their role in neural plasticity may provide insights into the maintenance of memory, and thus indicate clinical targets for the amelioration of age-related memory decline.

DAVID G. WELLS

BIBLIOGRAPHY

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