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Some of these interactions involve the upregulation of CD38, mediated by adipocyte-secreted angiotensin II (Ang II), which has been identified as the direct cause of increased expression of acetyl-CoA synthetase (ACSS2) in MM plasma cells, promoting growth by stabilizing the oncoprotein IRF4 in vitro and in vivo (95)

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The in-depth analyses of the results revealed that the proteins enolase, neuropolypeptide h3, ATP synthase, and fructose bis-aldolase (FBA) were identified as oxidized in brain from subjects at each stage of AD, late-stage AD, EAD, and MCI, consistent with the concept that their oxidation is an early event in and may contribute to progression of AD