Writing in the current Nature Neuroscience, Heather Cameron and Ronald D.G. McKay report that they were able to boost the rate of neurogenesis in the hippocampus of aging rats by lowering corticosteroid levels. The results support the hypothesis that the common memory decline of old age is a function of high corticosteroid (adrenal stress hormone) levels, and suggest that this decline could be reversed or prevented.

The interest in this relationship stems in part from findings that basal and stress-induced levels of corticosteroids are higher in both older rats and humans, and the finding that older humans who are able to avoid higher corticosteroid levels show no evidence of the usual age-related structural or functional changes in the hippocampus.

The authors reduced corticosteroid levels by adrenalectomy and found that cell proliferation in the subgranular zone of the dentate gyrus (where granule cell neurons are born) in aged animals increased dramatically, even above the levels found in young control rats. They were also able to confirm that the new cells differentiated into neurons and not into astrocytes.

If, in fact, the memory decline of aging (memory related to personal experience, or ‘episodic memory') is a function of an inadequate supply of new granule cells in the hippocampus, the implication of this study is that reducing corticosteroid levels could improve performance on the sorts of memory tasks associated with the hippocampus, namely episodic memory.—Hakon Heimer


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Primary Papers

  1. . Restoring production of hippocampal neurons in old age. Nat Neurosci. 1999 Oct;2(10):894-7. PubMed.