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Neurovascular MedicinePursuing Cellular Longevity for Healthy Aging$
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Kenneth Maiese

Print publication date: 2009

Print ISBN-13: 9780195326697

Published to Oxford Scholarship Online: January 2010

DOI: 10.1093/acprof:oso/9780195326697.001.0001

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Neurobiology of Postischemic Recuperation in the Aged Mammalian Brain

Neurobiology of Postischemic Recuperation in the Aged Mammalian Brain

(p.403) Chapter 17 Neurobiology of Postischemic Recuperation in the Aged Mammalian Brain
Neurovascular Medicine

Aurel Popa-Wagner

Adrian Balseanu

Leon Zagrean

Imtiaz M. Shah

Mario Di Napoli

Henrik Ahlenius

Zaal Kokaia

Oxford University Press

Old age is associated with an enhanced susceptibility to stroke and poor recovery from brain injury, but the cellular processes underlying these phenomena are not well understood. Potential mechanism underlying functional recovery after brain ischemia in aged subjects include neuroinflammation, changes in brain plasticity-promoting factors, unregulated expression of neurotoxic factors, or differences in the generation of scar tissue that impedes the formation of new axons and blood vessels in the infarcted region. Studies suggest that behaviorally, aged rats were more severely impaired by ischemia than were young rats and showed diminished functional recovery. Both in 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. Recent evidence shows that the human brain can respond to stroke with increased progenitor proliferation in aged patients, opening the possibilities of utilizing this intrinsic attempt for neuroregeneration of the human brain as a potential therapy for ischemic stroke.

Keywords:   ischemic stroke, neurotoxic factors, neuroregeneration, neurobiology, scar tissue, neuroinflammation, brain

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