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[DOI] [PubMed] [Google Scholar] 327.Cuadrado A., Martin-Moldes Z., Ye J., Lastres-Becker I

The subjects here exhibited relatively little cognitive deficit or mitochondrial dysfunction in the hippocampus, and their cognitive function was comparable to that of the control group that did not receive isoflurane.8 Alzheimers disease Mitochondrial dysfunction appears to be a central event in the pathogenesis of Alzheimers disease, so the preservation of mitochondrial health may be one of the keys to disease prevention.9 To that end, a 2017 study points favorably to SS-31s use for Alzheimers prevention

These together explain how Zebrin-II/ALDOC-positive Purkinje cells are selectively more vulnerable under ATM deficiency, and how specific anatomical degeneration due to the loss of these cells results in motor-related phenotypes in A-T