Short-term exposure to dim light at night disrupts rhythmic behaviors and causes neurodegeneration in fly models of tauopathy and Alzheimer's disease

Biochem Biophys Res Commun. 2018 Jan 8;495(2):1722-1729. doi: 10.1016/j.bbrc.2017.12.021. Epub 2017 Dec 5.

Abstract

The accumulation and aggregation of phosphorylated tau proteins in the brain are the hallmarks for the onset of Alzheimer's disease (AD). In addition, disruptions in circadian rhythms (CRs) with altered sleep-wake cycles, dysregulation of locomotion, and increased memory defects have been reported in patients with AD. Drosophila flies that have an overexpression of human tau protein in neurons exhibit most of the symptoms of human patients with AD, including locomotion defects and neurodegeneration. Using the fly model for tauopathy/AD, we investigated the effects of an exposure to dim light at night on AD symptoms. We used a light intensity of 10 lux, which is considered the lower limit of light pollution in many countries. After the tauopathy flies were exposed to the dim light at night for 3 days, the flies showed disrupted CRs, altered sleep-wake cycles due to increased pTau proteins and neurodegeneration, in the brains of the AD flies. The results indicate that the nighttime exposure of tauopathy/AD model Drosophila flies to dim light disrupted CR and sleep-wake behavior and promoted neurodegeneration.

Keywords: Alzheimer's disease (AD); Circadian rhythm (CR); Dim light at night (dLAN); Drosophila melanogaster; Neurodegeneration; Sleep.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / etiology*
  • Animals
  • Animals, Genetically Modified
  • Brain / metabolism
  • Brain / pathology
  • Circadian Rhythm / physiology
  • Circadian Rhythm / radiation effects*
  • Disease Models, Animal
  • Drosophila melanogaster / physiology
  • Drosophila melanogaster / radiation effects
  • Humans
  • Light
  • Longevity / genetics
  • Longevity / physiology
  • Male
  • Mutant Proteins / genetics
  • Mutant Proteins / metabolism
  • Nerve Degeneration / etiology*
  • Nerve Degeneration / metabolism
  • Nerve Degeneration / pathology
  • Photoperiod
  • Recombinant Proteins / genetics
  • Recombinant Proteins / metabolism
  • Sleep Wake Disorders / etiology
  • Tauopathies / etiology*
  • tau Proteins / genetics
  • tau Proteins / metabolism

Substances

  • MAPT protein, human
  • Mutant Proteins
  • Recombinant Proteins
  • tau Proteins