Neurons, glia, and plasticity in normal brain aging.
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 GFAP, may be a factor in impaired synaptic plasticity. Lastly, I discuss 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.
Finch
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CE
Andrus Gerontology Center, Dept Biological Sciences, University of Southern California, Los Angeles, CA 90089, USA. cefinch@usc.edu
D000375:Aging / Q000502:physiology*; D000818:Animals; D001921:Brain / Q000166:cytology / Q000502:physiology*; D006801:Humans; D009457:Neuroglia / Q000502:physiology*; D009473:Neuronal Plasticity; D009474:Neurons / Q000502:physiology*