Long-term exposure to constant light induces dementia, oxidative stress and promotes aggregation of sub-pathological Aβ42 in Wistar rats.

摘要: Abstract Constant exposure to light is prevalent in modern society where noise, shift work, and jet lag common. disrupts circadian rhythm, induces stress thus influences memory performance. We subjected adult male Wistar rats a two-month constant (LL), dark or normal light-dark cycles. Significant cognitive impairment oxidative were observed LL without significant elevation soluble Aβ1–42 levels. Next, we examined whether long-term may accelerate dementia sub-pathological Aβ model of rats. Normal control received ACSF, AD 440 pmol, (Aβ(s)) 220 pmol human Aβ42 peptide single unilateral ICV administration. Sub-pathological exposed (LL + Aβ(s)) show deficits damage, although not significantly different from Additionally, promoted aggregation exogenous LL + Aβ(s) shown by the presence congophilic plaques. Furthermore, chronic fluoxetine treatment (5 mg/kg/day) rescued behavioral deficits, damage amyloid aggregation. Whereas, rifampicin (20 mg/kg/day) did reverse but plaque formation. It was concluded that for two months stress, accelerates concentrations human-Aβ42 peptides rats, which reversed daily