Amyloid�β and tau are involved in sleep disorder in Alzheimer's disease by orexin�A and adenosine A(1) receptor
Amyloid-β and tau may contribute to sleep problems in Alzheimer's disease through orexin A and adenosine A1 receptor
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Abstract
Aβ25‑35 administration significantly decreased non‑rapid eye movement sleep and increased wakefulness in mice.
- Sleep disorder is confirmed as a core component of Alzheimer's disease.
- Increased levels of tau, phosphorylated tau (p‑tau), orexin A, and adenosine A1 receptor (A1R) were observed in the brains of Alzheimer's mice.
- In vitro studies showed similar increases in tau, p‑tau, orexin A, and A1R in human neuroblastoma cells treated with Aβ25‑35.
- The tau inhibitor TRx 0237 reversed the effects of Aβ25‑35 on tau, p‑tau, orexin A, and A1R expression levels.
- Knockdown of A1R or orexin A inhibited the increase in tau and p‑tau levels induced by Aβ25‑35.
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