Lifelong corticosterone level determines age-related decline in neurogenesis and memory.
Neurobiology of Aging. 2006-04-01; 27(4): 645-654
DOI: 10.1016/j.neurobiolaging.2005.02.014
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1. Neurobiol Aging. 2006 Apr;27(4):645-54. Epub 2005 Jun 13.
Lifelong corticosterone level determines age-related decline in neurogenesis and
memory.
Montaron MF(1), Drapeau E, Dupret D, Kitchener P, Aurousseau C, Le Moal M, Piazza
PV, Abrous DN.
Author information:
(1)Laboratoire de Physiopathologie du Comportement, I.N.S.E.R.M. Unité 588,
Université de Bordeaux II, Domaine de Carreire, 146, rue Léo. Saignat, 33077
Bordeaux Cedex, France.
Ageing is accompanied by an alteration of spatial memory, a decline in
hippocampal neurogenesis and a dysregulation of the hypothalamic-pituitary axis
(HPA) leading to elevated levels of circulating corticosterone. However, the role
of the HPA axis in age-related decline in cognitive functions and in neurogenesis
decline remains unclear. We found that suppression of glucocorticoids secretion
from midlife to the rest of the animals’ life increases neurogenesis in old
animals and prevents the emergence of age-related memory disorders. Reciprocally,
aged rats with a chronic upregulation of the HPA axis exhibit not only spatial
memory impairments but also very low levels of hippocampal cell proliferation and
survival. Altogether, these results indicate that the extent of lifetime exposure
to glucocorticoids determines the extent of age-related decline in hippocampal
neurogenesis and consequently age-related cognitive dysfunctions.
DOI: 10.1016/j.neurobiolaging.2005.02.014
PMID: 15953661 [Indexed for MEDLINE]