Circadian disruption resulting from exposure to irregular light–dark patterns and sleep deprivation has been associated with beta amyloid peptide (Aβ) aggregation, which is a major event in Alzheimer’s disease (AD) pathology. We exposed 5XFAD mice and littermate controls to dim-light vs. bright-light photophases to investigate the effects of altering photophase strength on AD-associated differences in cortical Aβ42 levels, wheel-running activity, and circadian free-running period (tauDD). We found that increasing light levels significantly reduced cortical Aβ42 accumulation and activity levels during the light phase of the light:dark cycle, the latter being consistent with decreased sleep fragmentation and increased sleep duration for mice exposed to the more robust light–dark pattern. No significant changes were observed for tauDD. Our results are consistent with circadian pacemaker period being relatively unaffected by Aβ pathology in AD, and with reductions in cortical Aβ loads in AD through tailored lighting interventions.

暴露于不规则的明暗模式和睡眠剥夺导致的昼夜节律紊乱与 β 淀粉样肽 (Aβ) 聚集有关，这是阿尔茨海默病 (AD) 病理学中的一个主要事件。我们将 5XFAD 小鼠和同窝对照暴露于弱光与强光光相位，以研究改变光相位强度对 AD 相关差异的皮质 Aβ42 水平、车轮运行活动和昼夜节律自由运行期 (tauDD) 的影响。我们发现，在光：暗周期的光阶段，增加光照水平显着降低了皮质 Aβ42 的积累和活动水平，后者与暴露于更强大的明暗模式的小鼠的睡眠碎片减少和睡眠持续时间增加一致。tauDD 没有观察到显着变化。