PuSH - Publikationsserver des Helmholtz Zentrums München: Inhalational anesthetics do not deteriorate amyloid-β-derived pathophysiology in alzheimer's disease: Investigations on the molecular, neuronal, and behavioral level.

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Hofmann, C.* ; Sander, A.* ; Wang, X.X.* ; Buerge, M.* ; Jungwirth, B.* ; Borgstedt, L.* ; Kreuzer, M.* ; Kopp, C.* ; Schorpp, K.K. ; Hadian, K. ; Wotjak, C.T.* ; Ebert, T.* ; Ruitenberg, M.* ; Parsons, C.G.* ; Rammes, G.*

Inhalational anesthetics do not deteriorate amyloid-β-derived pathophysiology in alzheimer's disease: Investigations on the molecular, neuronal, and behavioral level.

J. Alzheimers Dis. 84, 1193-1218 (2021)

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BACKGROUND: Studies suggest that general anesthetics like isoflurane and sevoflurane may aggravate Alzheimer's disease (AD) neuropathogenesis, e.g., increased amyloid-β (Aβ) protein aggregation resulting in synaptotoxicity and cognitive dysfunction. Other studies showed neuroprotective effects, e.g., with xenon. OBJECTIVE: In the present study, we want to detail the interactions of inhalational anesthetics with Aβ-derived pathology. We hypothesize xenon-mediated beneficial mechanisms regarding Aβ oligomerization and Aβ-mediated neurotoxicity on processes related to cognition. METHODS: Oligomerization of Aβ 1-42 in the presence of anesthetics has been analyzed by means of TR-FRET and silver staining. For monitoring changes in neuronal plasticity due to anesthetics and Aβ 1-42, Aβ 1-40, pyroglutamate-modified amyloid-(AβpE3), and nitrated Aβ (3NTyrAβ), we quantified long-term potentiation (LTP) and spine density. We analyzed network activity in the hippocampus via voltage-sensitive dye imaging (VSDI) and cognitive performance and Aβ plaque burden in transgenic AD mice (ArcAβ) after anesthesia. RESULTS: Whereas isoflurane and sevoflurane did not affect Aβ 1-42 aggregation, xenon alleviated the propensity for aggregation and partially reversed AβpE3 induced synaptotoxic effects on LTP. Xenon and sevoflurane reversed Aβ 1-42-induced spine density attenuation. In the presence of Aβ 1-40 and AβpE3, anesthetic-induced depression of VSDI-monitored signaling recovered after xenon, but not isoflurane and sevoflurane removal. In slices pretreated with Aβ 1-42 or 3NTyrAβ, activity did not recover after washout. Cognitive performance and plaque burden were unaffected after anesthetizing WT and ArcAβ mice. CONCLUSION: None of the anesthetics aggravated Aβ-derived AD pathology in vivo. However, Aβ and anesthetics affected neuronal activity in vitro, whereby xenon showed beneficial effects on Aβ 1-42 aggregation, LTP, and spine density.

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