Melatonin-mediated calcineurin inactivation attenuates amyloid beta-induced apoptosis.
IBRO Neurosci Rep
; 16: 336-344, 2024 Jun.
Article
em En
| MEDLINE
| ID: mdl-38390232
ABSTRACT
Alzheimer's disease (AD) is the most common age-related progressive neurodegenerative disorder. The accumulation of amyloid beta-peptide is a neuropathological marker of AD. While melatonin is recognized to have protective effects on aging and neurodegenerative disorders, the therapeutic effect of melatonin on calcineurin in AD is poorly understood. In this study, we examined the effect and underlying molecular mechanisms of melatonin treatment on amyloid beta-mediated neurotoxicity in neuroblastoma cells. Melatonin treatment decreased calcineurin and autophagy in neuroblastoma cells. Electron microscopy images showed that melatonin inhibited amyloid beta-induced autophagic vacuoles. The increase in the amyloid beta-induced apoptosis rate was observed more in PrPC-expressing ZW cells than in PrPC-silencing Zpl cells. Taken together, the results suggest that by mitigating the effect of calcineurin and autophagy flux activation, melatonin could also rescue amyloid beta-induced neurotoxic effects. These findings may be relevant to therapy for neurodegenerative diseases, including AD.
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1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
IBRO Neurosci Rep
Ano de publicação:
2024
Tipo de documento:
Article