Testosterone May Hold Therapeutic Promise for the Treatment of Ischemic Stroke in Aging

madman

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Testosterone May Hold Therapeutic Promise for the Treatment of Ischemic Stroke in Aging: A Closer Look at Laboratory Findings

Fereshteh Farajdokht, Mehdi Farhoudi, Alireza Majdi, Masumeh Zamanlu, Saeed Sadigh-Eteghad, Shabnam Vahedi, Javad Mahmoudi*







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














Conclusion
Based on above, TES neuroprotection against stroke in aging appears to be mediated by several mechanisms including inhibition of production of oxidant molecules, enhancing the enzymatic antioxidant capacity of the brain, activation of PI3K/AKT pathway and enhancing cell survival, inhibition of pro-apoptotic protein through AR dependent MAPK/ERK pathway, as well as improvement of brain neuronal and BBB integrities. These mechanisms may propose future therapeutic strategies to improve the quality of life and decrease androgen-related health problems in the aging population.
 

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Screenshot (145).webp

Figure 1. The essential molecular components of testosterone biosynthesis in Leydig cells and the inhibitory effects of aging at multiple levels on these machineries. LH: luteinizing hormone; StAR: steroidogenic acute regulatory protein; TSPO: translocator protein; PKA: protein kinase A; CYP17: 17α-hydroxylase/C17-20 lyase
 
Screenshot (146).webp

Figure 2. Ischemic stroke triggers cascades of complex events resulting in the neuronal loss in affected area. Testosterone induces neuroprotection in the neuronal cell following cerebral ischemia through inhibition of oxidative stress and blocking apoptotic cell death. ROS: reactive oxygen species; TES: testosterone; MAPK: mitogen-activated protein kinase; ERK: extracellular signalregulated protein kinase.
 
Testosterone May Hold Therapeutic Promise for the Treatment of Ischemic Stroke in Aging: A Closer Look at Laboratory Findings

Fereshteh Farajdokht, Mehdi Farhoudi, Alireza Majdi, Masumeh Zamanlu, Saeed Sadigh-Eteghad, Shabnam Vahedi, Javad Mahmoudi*







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














Conclusion
Based on above, TES neuroprotection against stroke in aging appears to be mediated by several mechanisms including inhibition of production of oxidant molecules, enhancing the enzymatic antioxidant capacity of the brain, activation of PI3K/AKT pathway and enhancing cell survival, inhibition of pro-apoptotic protein through AR dependent MAPK/ERK pathway, as well as improvement of brain neuronal and BBB integrities. These mechanisms may propose future therapeutic strategies to improve the quality of life and decrease androgen-related health problems in the aging population.


Curious since there are guys only injecting testosterone what happens to the LH receptors?
It appears the article indicates you need Lh for this benefit. I'll be honest I skimmed through it.
 

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