Constant exposure to light is prevalent in modern society where light noise, shift work, and jet lag is common. Constant light exposure disrupts circadian rhythm, induces stress and thus influences memory performance. We subjected adult male Wistar rats to a two-month exposure to constant light (LL), constant dark or normal light-dark cycles. Significant cognitive impairment and oxidative stress were observed in LL rats without a significant elevation in soluble Aβ_1–42 levels. Next, we examined whether long-term exposure to constant light may accelerate dementia in a sub-pathological Aβ model of rats. Normal control rats received ACSF, AD rats received 440 pmol, and sub-pathological Aβ rats (Aβ_(s)) received 220 pmol of human Aβ₄₂ peptide in a single unilateral ICV administration. Sub-pathological Aβ rats exposed to constant light (LL + Aβ_(s)) show significant memory deficits and oxidative damage, although not significantly different from LL rats. Additionally, constant light promoted aggregation of exogenous Aβ₄₂ in LL + Aβ_(s) rats shown by the presence of congophilic plaques. Furthermore, chronic fluoxetine treatment (5 mg/kg/day) rescued rats from the behavioral deficits, oxidative damage and amyloid aggregation. Whereas, rifampicin treatment (20 mg/kg/day) did not reverse the behavioral deficits or oxidative stress but rescued rats from amyloid plaque formation. It was concluded that constant light for two months induces behavioral deficits, oxidative stress, and accelerates aggregation of sub-pathological concentrations of human-Aβ₄₂ peptides in Wistar rats, which is reversed by daily fluoxetine administration.

在现代社会中，经常暴露于光线是普遍的问题，在现代社会中，噪声，轮班工作和时差是很普遍的。持续不断的曝光会破坏昼夜节律，诱发压力并因此影响记忆性能。我们对成年雄性Wistar大鼠进行了两个月的持续光照（LL），持续黑暗或正常光照-黑暗周期的暴露。在LL大鼠中观察到显著认知损伤和氧化应激而没有可溶性Aβ一个显著海拔_{1 - 42级}水平。接下来，我们检查了长期暴露于恒定光下是否会在大鼠亚病理Aβ模型中加速痴呆。接收ACSF正常对照组大鼠，AD大鼠接受440皮摩尔和子病理Aβ大鼠（Aβ _（S） ）接受220皮摩尔人类的Aβ ₄₂一次单方ICV给药中的多肽。暴露于恒定光（LL +Aβ _（s））的亚病理Aβ大鼠显示出明显的记忆缺陷和氧化损伤，尽管与LL大鼠没有显着差异。此外，恒定的光促进外源Aβ的聚集₄₂在LL +Aβ _（S）大鼠表现出嗜血菌斑。此外，慢性氟西汀治疗（5 mg / kg /天）使大鼠摆脱了行为缺陷，氧化损伤和淀粉样蛋白聚集。利福平治疗（20 mg / kg /天）并不能逆转行为缺陷或氧化应激，但可以挽救大鼠淀粉样斑块的形成。结论是，持续光照两个月会诱发行为缺陷，氧化应激并加速Wistar大鼠中人_Aβ42肽亚病理浓度的聚集，这可通过每天服用氟西汀来逆转。