Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication

DOI

10.1016/j.neurobiolaging.2005.02.014

Type

Journal article

Journal

Neurobiol Aging

Publication Date

04/2006

Volume

27

Pages

645 - 654

Keywords

Adrenal Glands, Adrenalectomy, Age Factors, Aging, Analysis of Variance, Animals, Behavior, Animal, Bromodeoxyuridine, Cell Count, Corticosterone, Immunohistochemistry, Ki-67 Antigen, Male, Maze Learning, Memory Disorders, Models, Biological, Neurons, Organ Size, Organogenesis, Rats, Rats, Sprague-Dawley, Reaction Time, Statistics as Topic, Stereotaxic Techniques, Stress, Physiological