Ischemic
white matter damage (WMD) is increasingly being considered as one of
the major causes of neurological disorders in older adults and preterm
infants. The functional consequences of WMD triggers a progressive
cognitive decline and dementia particularly in patients with ischemic
cerebrovascular diseases. Despite the major stride made in the
pathogenesis mechanisms of ischemic WMD in the last century, effective
medications are still not available. So, there is an urgent need to
explore a promising approach to slow the progression or modify its
pathological course. In this review, we discussed the animal models, the
pathological mechanisms and the potential therapeutic agents for
ischemic WMD. The development in the studies of anti-oxidants, free
radical scavengers, anti-inflammatory or anti-apoptotic agents and
neurotrophic factors in ischemic WMD were summarized. The agents which
either alleviate oligodendrocyte damage or promote its proliferation or
differentiation may have potential value for the treatment of ischemic
WMD. Moreover, drugs with multifaceted protective activities or a wide
therapeutic window may be optimal for clinical translation.
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