Aging Rewires Neuronal Metabolism, Exacerbating Cell Death After Ischemic Stroke: A Hidden Reason for the Failure of Neuroprotection.

Matvey Vadyukhin, Vladimir Shchekin, Petr Shegai, Andrey Kaprin, Grigory Demyashkin

Department of Digital Oncomorphology, National Medical Research Centre of Radiology, 2nd Botkinsky Pass., 3, 125284 Moscow, Russia. · pubmed

Paper

Abstract

Aging profoundly modifies neuronal responses to ischemia. We aimed to define age-dependent features of neuronal metabolism and cell death after ischemic stroke by assessing NeuN, NSE, and Caspase-3 in human cortical neurons and by comparing transcriptional activity within PI3K/Akt/mTOR and PI3K/Akt/FOXO3a pathways across age groups. The aim of this study was to determine age-dependent features of neuronal metabolism and cellular degradation in ischemic stroke based on immunohistochemical assessment of NeuN, NSE, and Caspase-3 markers in human cerebral cortex neurons, as well as to conduct a comparative analysis of gene expression in the PI3K/Akt/mTOR and PI3K/Akt/FOXO3a signaling pathways involved in the regulation of neuronal survival and apoptosis. For the investigation, frontal cortex autopsies from patients with ischemic stroke (

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Research summary

Aging modifies neuronal metabolism and exacerbates cell death after ischemic stroke. The study addresses age-dependent mechanisms that contribute to neuronal degradation, which is crucial for understanding the underlying processes of aging and potential interventions.

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