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    Neurobiol Aging. 2003 May-Jun;24 Suppl 1:S123-7; discussion S131.

    Neurons, glia, and plasticity in normal brain aging.

    Source

    Department of Biological Sciences, Ethel Percy Andrus Gerontology Center, University of Southern California, 3715 McClintock Avenue, Los Angeles, CA 90089-0191, USA. cefinch@usc.edu

    Abstract

    Early manifestations of brain aging have received much less attention than the drastic degeneration of AD and MID. During nonpathological changes of normal aging, brain systems differ in the involvement of neuron loss. Spatial learning can become impaired without evidence for neuron loss, whereas eye-blink conditioning deficits are well correlated with Purkinje neuron loss. Glial activation, in particular the increased expression of glial fibrillary acidic protein (GFAP), may be a factor in impaired synaptic plasticity. Lastly, it is discussed how developmental variations in the numbers of Purkinje cells and ovarian oocytes can be factors in outcomes of aging that are not under strict genetic control.

    PMID:
    12829120
    [PubMed - indexed for MEDLINE]

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