CHSJ

Curr Health Sci J, vol. 35, no. 4, 2009

Cellular Responses to Cerebral Ischemia during Aging

[Original paper]

T.A. BALSEANU(1) (2), A.M. BUGA(1)(2), A. POPA-WAGNER(1)(2)


(1)Dept. of Neurology, University of Greifswald, Germany;
(2)Department of Molecular Medicine, University of Medicine and Pharmacy Craiova, Romania


Abstract:

Old age is associated with an enhanced susceptibility to stroke and poor recovery from brain injury, but the cellular processes underlying these phenomena are uncertain. Therefore studying the basic mechanism underlying functional recovery after brain ischemia in aged subjects is of considerable clinical interest. The available evidence indicates that (i) compared to young rats, middle aged rats develop a larger infarct area, as well as a necrotic zone characterized by a higher rate of cellular degeneration, and a larger number of apoptotic cells; (ii) in both old and young rats, the early intense proliferative activity following stroke leads to a precipitous formation of growth-inhibiting scar tissue, a phenomenon amplified by the persistent expression of neurotoxic factors; and (iii) the regenerative potential of the rat brain is largely preserved up to 20 months of age but gene expression temporally displaced, has a lower amplitude, and is sometimes of relatively short duration. Whether endogenous neurogenesis contributes to spontaneous recovery after stroke has not yet been established. If the neurogenesis from endogenous NSCs will be used as therapeutic approach, it will require individual approach to assess the possible extent of neurogenic response and possibilities to alter this response for functional improvement or prevention of further progression of the disease.


Keywords: stroke, aging, recuperation; glial scar; degeneration; apoptosis; microglia activation; cytoproliferation; regeneration; neurogenesis



Corresponding: Aurel Popa-Wagner, Ph.D.; Department of Neurology; University of Greifswald; Ellernholzstr. 1-2; 17487 Greifswald; Germany; Fax: 03834-866876; e-mail: wagnerap@uni-greifswald.de


DOI 10.12865/CHSJ.35.04.01 - Download PDF
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