Abstract
Male sex is more prone to cerebrovascular disorders, yet the exact role of androgens in cerebral ischemia remains unclear. Here we reviewed current understanding of testosterone (TES) neuroprotective activity against ischemic stroke and mechanisms underlying these effects in aging. TES may exert a neuroprotective effect in aging through pathways including inhibition of oxidant molecules production, enhancing the enzymatic antioxidant capacity of the brain and modulation of apoptotic cell death. Given this, a better understanding of the neuroprotective roles of TES may propose an effective therapeutic strategy to improve the quality of life and decrease androgen-related cerebrovascular problems in the aging men.
Highlights
Stroke is a highly disabling cerebrovascular disease among the elderlies associating with significant mortality and morbidity and considerable economic burden.[1]
Male sex is more prone to cerebrovascular disorders, yet the exact role of androgens in cerebral ischemia remains unclear
We reviewed current understanding of testosterone (TES) neuroprotective activity against ischemic stroke and mechanisms underlying these effects in aging
Summary
Stroke is a highly disabling cerebrovascular disease among the elderlies associating with significant mortality and morbidity and considerable economic burden.[1]. Male sex is considered as an important risk factor for stroke. In comparison with age-matched women, the overall incidence of stroke in men is high indicating that sex steroids may have a role in the pathophysiology of stroke.[5] There is a link between low circulating testosterone (TES) levels and incidence of cerebrovascular events such as transient ischemic attack and ischemic stroke in men. Low levels of TES appears to be involved in clinical outcomes of ischemic stroke survivors.[6,7] some of the major stroke risk factors such as cardiovascular disorders,[8] atherosclerosis[9] and type 2 diabetes[10] are usually associated with low TES levels in the old men. Given the role of TES in stroke, this paper aims to focus on the different neuroprotective mechanisms of TES in ischemic stroke
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