Near-infrared light reduces glia activation and modulates neuroinflammation in the brains of diet-induced obese mice

Abstract

Neuroinflammation is a key event in neurodegenerative conditions such as Alzheimer’s disease (AD) and characterizes metabolic pathologies like obesity and type 2 diabetes (T2D). Growing evidence in humans shows that obesity increases the risk of developing AD by threefold. Hippocampal neuroinflammation in rodents correlates with poor memory performance, suggesting that it contributes to cognitive decline. Here we propose that reducing obesity/T2D-driven neuroinflammation may prevent the progression of cognitive decline associated with AD-like neurodegenerative states. Near-infrared light (NIR) has attracted increasing attention as it was shown to improve learning and memory in both humans and animal models. We previously reported that transcranial NIR delivery reduced amyloid beta and Tau pathology and improved memory function in mouse models of AD. Here, we report the effects of NIR in preventing obesity-induced neuroinflammation in a diet-induced obese mouse model. Five-week-old wild-type mice were fed a high-fat diet (HFD) for 13 weeks to induce obesity prior to transcranial delivery of NIR for 4 weeks during 90-s sessions given 5 days a week. After sacrifice, brain slices were subjected to free-floating immunofluorescence for microglia and astrocyte markers to evaluate glial activation and quantitative real-time polymerase chain reaction (PCR) to evaluate expression levels of inflammatory cytokines and brain-derived neurotrophic factor (BDNF). The hippocampal and cortical regions of the HFD group had increased expression of the activated microglial marker CD68 and the astrocytic marker glial fibrillary acidic protein. NIR-treated HFD groups showed decreased levels of these markers. PCR revealed that hippocampal tissue from the HFD group had increased levels of pro-inflammatory interleukin (IL)-1β and tumor necrosis factor-α. Interestingly, the same samples showed increased levels of the anti-inflammatory IL-10. All these changes were attenuated by NIR treatment. Lastly, hippocampal levels of the neurotrophic factor BDNF were increased in NIR-treated HFD mice, compared to untreated HFD mice. The marked reductions in glial activation and pro-inflammatory cytokines along with elevated BDNF provide insights into how NIR could reduce neuroinflammation. These results support the use of NIR as a potential non-invasive and preventive therapeutic approach against chronic obesity-induced deficits that are known to occur with AD neuropathology.

PBM Combined with hUCMSCs Modulates the Polarization of Microglia

“…The application of 810 nm light was able to promote the recovery of motor function in spinal cord-injured mice, reduce apoptosis, inhibit neurotoxic microglia activation and alleviate neuroin ammation [16]. NIR light has been shown to enhance learning and memory in both human and animal models [40,41]. Moreover, treatment with coenzyme Q10 and 810 nm light alone or together has the ability to boost cognitive function, decrease levels of TNF-α and IL-1β, and alleviate neuroin ammation in mice with cerebral ischemia [42].…”

Use of either transcranial or whole‐body photobiomodulation treatments improves COVID‐19 brain fog

“…Finally, an extracellular PBM mechanism involving direct activation of latent TGF-β1 involving a redoxmediated conformational change has been described [99]. The role of these specific pathways to enable improved neuroplasticity and reduced neuroinflammation has contributed to improved cognition [100][101][102].…”

Astragalus polysaccharides ameliorate epileptogenesis, cognitive impairment, and neuroinflammation in a pentylenetetrazole-induced kindling mouse model

“…Higher pro-inflammatory cytokine expression is another important feature of neuroinflammation that occurs along with glial activation (Saieva and Taglialatela, 2022). To determine the effect of APS on pro-inflammatory cytokines in PTZ-induced kindling in mice, we detected the levels of TNF-α, IL-1β, and IL-6 in the hippocampus and cortex using ELISA kits (Figure 9).…”