http://link.springer.com/chapter/10.1007/978-1-4614-9123-1_9
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Abstract
In chronic cerebral
hypoperfusion due to aging, global cerebral ischemia after cardiac
arrest, acute and chronic hypoxia in asymptomatic stroke, and diffuse
axonal injury after traumatic brain injury, white matter lesions occur
not only as a result of secondary degeneration caused by neuronal
injuries in the gray matter, but also as a direct consequence of the
primary ischemic insults. Not enough attention has been directed to the
molecular and cellular mechanisms of white matter injuries in humans.
Failures in past stroke therapyclinical trials are partly attributed to
misrepresentation of the relevance of white matter to human brain
pathology in the preclinical data. Most rodent models either ignore
white matter's contribution to the injury process and recovery, or
inadequately account for this contribution due to a significantly lower
proportion of white matter in the rodent brain compared to the human
brain. Future development of effective therapies should place an equal
emphasis on gray and white matter injuries.
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