Artificial light and neurodegeneration: does light pollution impact the development of Alzheimer's disease?

Abstract

Two multidimensional problems of recent times - Alzheimer's disease and light pollution - seem to be more interrelated than previously expected. A series of studies in years explore the pathogenesis and the course of Alzheimer's disease, yet the mechanisms underlying this pathology remain not fully discovered and understood. Artificial lights which accompany civilization on a daily basis appear to have more detrimental effects on both environment and human health than previously anticipated. Circadian rhythm is affected by inappropriate lighting conditions in particular. The consequences are dysregulation of the sleep-wake cycle, gene expression, neuronal restructuring, brain's electricity, blood flow, metabolites' turnover, and gut microbiota as well. All these phenomena may contribute to neurodegeneration and consequently Alzheimer's disease. There is an increasing number of research underlining the complexity of the correlation between light pollution and Alzheimer's disease; however, additional studies to enhance the key tenets are required for a better understanding of this relationship.

Keywords: Alzheimer’s disease; Circadian rhythm; Dementia; Light pollution; Neurodegeneration.

Fig. 1

The potential mechanisms of AD development. Under conditions of circadian rhythm disruption, there is an accumulation of neurotoxic proteins that are not removed from brain tissue via glial phagocytosis or active transport. These processes are intensified by high orexin levels and disrupted melatonin releasing patterns. Moreover, impairment of melatonin release leads to more excellent production of Aβ [13, 15, 24, 25, 38]

Fig. 2

Relations between genes responsible for circadian rhythm and neurodegeneration are numerous. Deleting the BMAL1 center clock’s gene in the cortex and hippocampus leads to oxidative stress including severe reactive astrocytosis, neuronal oxidative damage, the degeneration of synaptic terminals, and neurodegeneration. In turn, neurodegenerative protein Aβ triggers deterioration of BMAL1 and CBP center clock proteins which then change the expression of BMAL1 and PER2 center clock’s genes resulting in a disturbed circadian rhythm. BMAL1 and CLOCK proteins also activate PSEN-2 gene expression which codes presenilin-2 protein. This protein cleaves APP and, as a result, diminishes the amount of Aβ [11, 22, 39, 40]