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In mammals, mitochondrially-localised PRX3 is predicted to compensate PRX5 functioning (Table 1) 53 , and D

CGM can be used as a crucial monitoring tool and its use should be encouraged in IAS patients to prevent life-threatening episodes of hypoglycemia

Altogether, these multifaceted mitochondrial alterations would be expected to lead to a series of energetically costly adjustments, including compensatory hypermetabolism in the thalamus and cerebellum [152]

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The authors suggest that their studies provide insights into A42 and brain insulin resistance as a significant contributing component of the pathophysiology of AD (180)

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