Tau Contributes to Sevoflurane-induced Neurocognitive Impairment in Neonatal Mice

ConclusionsHigher brain Tau concentrations and lower brain mitochondrial metabolism in neonatal compared with adult mice contribute to developmental stage –dependent cognitive dysfunction after sevoflurane anesthesia.Editor ’s PerspectiveWhat We Already Know about This TopicPathologic aggregation of the neuronal microtubule-associated protein Tau is a hallmark of Alzheimer ’s diseaseSevoflurane anesthesia induces Tau phosphorylation and cognitive impairment in neonatal but not in adult mice, but the molecular mechanisms underlying these age-dependent effects have not been previously reportedWhat This Article Tells Us That Is NewNeonatal mice have higher brain Tau levels and higher brain concentrations of Nuak1, an enzyme that phosphorylates Tau, when compared with adult counterpartsNeonatal mice have decreased mitochondrial activity and lower brain ATP concentrations when compared with adult counterpartsPharmacologic inhibition of Tau phosphorylation or enhancement of mitochondrial function in neonatal mice protects against sevoflurane anesthesia –induced cognitive deficitsThese observations suggest that developmental stage –dependent differences in mitochondrial activity and Tau phosphorylation can render neonatal mice more vulnerable to the development of Tauopathy and cognitive impairment after sevoflurane anesthesia

Source: Anesthesiology - July 14, 2020 Category: Anesthesiology Source Type: research