# Transcranial Irradiation Mitigates Paradoxical Sleep Deprivation Effect in an Age-Dependent Manner: Role of BDNF and GLP-1

## TL;DR

This study shows that transcranial near-infrared light helps reduce cognitive issues caused by sleep deprivation in young but not old rats, possibly by boosting brain chemicals like BDNF and GLP-1.

## Contribution

The study reveals age-dependent effects of NIR light on mitigating sleep deprivation-induced cognitive decline and identifies BDNF and GLP-1 as key factors.

## Key findings

- NIR photobiomodulation improved cognition in young but not senile sleep-deprived rats.
- NIR reduced anxiety-like behavior in both young and old sleep-deprived rats.
- NIR increased BDNF and GLP-1 mRNA in senile rats, promoting neuronal survival.

## Abstract

The growing prevalence of aged sleep-deprived nations is turning into a pandemic state. Acute sleep deprivation (SD) accompanies aging, changing the hippocampal cellular pattern, neurogenesis pathway expression, and aggravating cognitive deterioration. The present study investigated the ability of Near Infra Red (NIR) light laser to ameliorate cognitive impairment induced by SD in young and senile rats. Wistar rats ≤ 2 months (young) and ≥ 14 months (senile) were sleep-deprived for 72 h with or without transcranial administration of NIR laser of 830 nm. Our results showed that NIR photobiomodulation (PBM) attenuated cognitive deterioration made by SD in young, but not senile rats, while both sleep-deprived young and senile rats exhibited decreased anxiety (mania)-like behavior in response to PBM. NIR PBM had an inhibitory effect on AChE, enhanced the production of ACh, attenuated ROS, and regulated cell apoptosis factors such as Bax and Bcl-2. NIR increased mRNA expression of BDNF and GLP-1 in senile rats, thus facilitating neuronal survival and differentiation. The present findings also revealed that age exerts an additive factor to the cellular assaults produced by SD where hippocampal damages made in 2-month rats were less severe than those of the aged one. In conclusion, NIR PBM seems to promote cellular longevity of senile hippocampal cells by combating ROS, elevating neurotrophic factors, thus improving cognitive performance. The present findings provide NIR as a possible candidate for hippocampal neuronal insults accompanying aging and SD.

The online version contains supplementary material available at 10.1007/s11064-023-04071-y.