Abstract

This study explored the effects of long-term photobiomodulation (PBM) on the glial and neuronal organization in the striatum of aged mice. Mice aged 12 months were pretreated with PBM (670 nm) for 20 minutes per day, commencing at 5 months old and continued for 8 months. We had 2 control groups, young at 3 months and aged at 12 months old; these mice received no treatment. Brains were aldehyde-fixed and processed for immunohistochemistry with various glial and neuronal markers. We found a clear reduction in glial cell number, both astrocytes and microglia, in the striatum after PBM in aged mice. By contrast, the number of 2 types of striatal interneurons (parvalbumin+ and encephalopsin+), together with the density of striatal dopaminergic terminals (and their midbrain cell bodies), remained unchanged after such treatment. In summary, our results indicated that long-term PBM had beneficial effects on the aging striatum by reducing glial cell number; and furthermore, that this treatment did not have any deleterious effects on the neurons and terminations in this nucleus.

Highlights

  • A characteristic feature of the central nervous system in aging is an activation of glial cells (Lynch et al, 2014; Soreq et al, 2017)

  • All experiments were approved by the Animal Ethics Committee of the University College London and Home Officeelicensed procedures conforming to the UK Animal Licence Act (1986)

  • Our results indicated that in mice aged 12 months, PBM had a greater impact on reducing glial numbers than on increasing neuronal ones; and that this treatment had no deleterious effects on either type of brain cells

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Summary

Introduction

A characteristic feature of the central nervous system in aging is an activation of glial cells (Lynch et al, 2014; Soreq et al, 2017). Many previous studies have reported a marked increase in the number of glial cells due to aging, both astrocytes and microglia, across the central nervous system (Beach et al, 1989; Unger, 1998). A further feature of aging is that, in contrast to the increase in glial cell number, there is a progressive loss of neurons This loss manifests after a series of intrinsic molecular changes within the neurons leading to dysfunction and death. Such changes render aging neurons more susceptible to insult, whether by environmental toxin or genetic mutation, such as in Alzheimer’s or Parkinson’s disease. Aging is a major risk factor for both these neurodegenerative disorders (Balaban et al, 2005; Kujoth et al, 2005; Linnane et al, 1989; Salvadores et al, 2017)

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