engleski

Prevention and treatment of vascular dementia: exploring the neuroprotective potential of dehydroepiandrosterone (DHEA) and DHEA sulphate /DHEAS) in vitro.

Ischemic brain injury and cerebrovascular disease are common causes of cognitive decline and dementia in the elderly [1]. Vascular dementia (VaD) is the second most common cause of dementia in the elderly population after Alzheimer’ disease. VaD is caused by reduced blood flow to the various brain regions, depriving them of oxygen and nutrients and causing neurodegeneration and cell death [2]. Neurosteroids dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) are the most abundant steroid hormones and can be synthesized de novo in the brain [3]. They have been shown to be potent modulators of neurogenesis, neuronal metabolism and neuroprotection [4]. Previous research has shown that these neurostreoids alleviate the effects of excitotoxicity and damage caused by oxidative stress and have potentially protective effects in the case of ischemic brain injury [5]. The aim of this study was to investigate the potential neuroprotective effects of DHEA and DHEAS using an oxygen and glucose deprivation and reperfusion (OGD/R) model that mimics ischemic injury and related pathological conditions. Oxygen-glucose deprivation (OGD) was performed in primary mouse neurons derived from C57BL/6 mice, and human SH- SY5Y neuroblastoma cells as an in vitro model of VaD. Both cell cultures were treated with DHEA and DHEAS 24 hours before injury (pretreatment) or 24 hours after injury (posttreatment) and cell viability and oxidative stress parameters were determined. The obtained results demonstrated beneficial effects of DHEA and DHEAS treatment on cell survival and viability, suggesting potential neuroprotective actions of these neurosteroids in VaD.

Vascular dementia ; DHEA(S) ; OGD

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