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Abstract Background The pathogenic mechanisms of vascular cognitive impairment (VCI) are complicated, involving brain atrophy, parenchymal damage, and functional dysconnectivity associated with vascular risk factors, cerebrovascular diseases, and mixed pathologies

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In FoB, we found that ATP levels in Gclc -deficient, but not in Gclc -sufficient FoB dropped in a dose-dependent fashion in response to inhibition of glycolysis with 2-deoxy-D-glucose (2-DG) or galactose (Fig

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10.1155/2017/9831534 [DOI] [PMC free article] [PubMed] [Google Scholar] Gjorevski N., Sachs N., Manfrin A., Giger S., Bragina M