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Could a type of phototherapy delivered during sleep help treat Alzheimer’s disease? Design by MNT; Photography by Halfpoint Images/Getty Images & Ping Shu/Getty Images.
  • Amidst the rising global prevalence of Alzheimer’s disease, linked to increasing life expectancies, finding effective treatments has never been more critical, especially given the current lack of efficacious drug-based solutions.
  • New research reveals that photobiomodulation (PBM), a nonpharmacological approach, has demonstrated promising initial results in both human and animal studies, particularly when applied during sleep, acting like a ‘washing machine’ for the brain to enhance the removal of harmful beta-amyloid proteins.
  • These discoveries not only shed light on the potential of PBM and the underlying restorative functions of sleep but also pave the way for the development of innovative technologies aiming to leverage sleep for Alzheimer’s disease therapy.

Adequate sleep is essential for good health, but the reasons why the brain heals more effectively during sleep and whether these processes can be influenced is still unclear.

Research suggests that the brain’s lymphatic system is more active during sleep, aiding in eliminating waste products, toxins, and unnecessary molecules from brain tissues.

Disrupted sleep can lead to a build-up of these waste products in the central nervous system (CNS), and consequently, sleep has been identified as a biomarker for Alzheimer’s disease.

This relationship is attributed to the fact that the harmful metabolite beta-amyloid is expelled from the brain during sleep.

Lack of sleep results in the accumulation of this toxin in the CNS, potentially contributing to the onset of Alzheimer’s disease over time.

In a new study published in Frontiers of Optoelectronics, researchers demonstrated that a noninvasive technology called sleep photobiomodulation (PBM) could effectively enhance the removal of beta-amyloid from the brain tissues of mice.

Notably, the therapeutic impact of PBM was found to be more pronounced during sleep than when awake.

Applying PBM while sleeping essentially turns the brain into a “washing machine,” helping to clear out toxic beta-amyloid and boost the brain’s resistance to Alzheimer’s disease progression.

In this new research, scientists demonstrated that combining a special chemical, 5-aminolevulenic acid, with laser light at a specific wavelength reduces the network of vessels in the membranes covering the brain, which are called meningeal lymphatic vessels (MLVs).

This reduction leads to a decrease in the removal of a harmful protein beta-amyloid from specific areas of the brain.

Researchers employed a unique PBM protocol, where they monitored the mice’s brain activity during different stages of sleep and wakefulness without using anesthesia.

They discovered that applying PBM for 7 days during deep sleep was more effective in promoting the removal of the harmful proteins from the brain compared to when the mice were awake.

These findings help in understanding how PBM works and highlight its potential in stimulating the brain’s natural waste removal system, especially during sleep.

This discovery adds a new aspect to the study of how sleep can have restorative functions and offers a valuable foundation for developing innovative technologies focused on enhancing sleep for Alzheimer’s disease treatment.

Three experts, not involved in this research, spoke to Medical News Today about the study.

Dr. Rajkumar Dasgupta, a quadruple board certified physician and Chief Medical Advisor for Sleep Advisor, said that “the research exploring phototherapy, which is a nonpharmacologic treatment, is noninvasive and promising.”

“Drug treatment for dementia has limitations such as medical contraindications, limited efficacy, and adverse effects,” he noted, adding that “[r]esearch such as this, evaluating nonpharmacological therapy, has been increasingly regarded as a critical part of comprehensive dementia care.”

“Previous studies suggest that it could potentially benefit people with dementia and its symptoms, particularly in regards to improving cognition. However, [while] this research is well conducted in mice, […] [it] is still in its infancy and there is currently not enough evidence to recommend phototherapy as an intervention in individuals who suffer from dementia. More clinical studies in humans are needed to fully understand the benefit and potential side effects.”

– Dr. Rajkumar Dasgupta

Dr. Kezia Joy, a medical content advisor for Welzo, agreed, saying that “the findings presented in this study are intriguing and shed light on a potentially novel approach for the therapy of Alzheimer’s disease through photobiomodulation (PBM).”

However, “it’s important to note that while these findings are promising, further research, including clinical trials in humans, will be necessary to validate the safety and efficacy of PBM as a therapeutic approach for [Alzheimer’s disease],” Dr. Joy explained.

And Dr. Theodore Henderson, a psychiatrist based in Denver, CO, suggested that “the title [of the research study] is somewhat misleading.”

“This is a series of experiments to test the effects of infrared light photobiomodulation (PBM) on the recovery of damaged glial lymphatic drainage channels, referred to in the paper as meningeal lymphatic vessels (MLVs),” he said.

“The animals are standard laboratory mice, not genetically developed Alzheimer’s models. As such, the findings are limited to the question of what happens [when] the MLVs become damaged. The authors attempt to draw a line from the purported decreased clearance of toxins — beta-amyloid, in particular — in the Alzheimer’s state to the results of the ablation study. They neglect that other processes besides the accumulation of interstitial toxins are ongoing in and around the Alzheimer’s neuron[s], including mitochondrial dysfunction.”

– Dr. Theodore Henderson

“All that aside, this group shows that they can injure or damage the MLVs with a photosensitive toxin which is activated by red light,” Dr. Henderson said. “The group has shown that damaging the MLVs reduce the clearance of beta amyloid from otherwise healthy mice.”

Dr. Henderson concluded: “I would have liked to have seen this study done in a mouse model of Alzheimer’s disease.”

The research continues, however, this novel approach could offer a potential new treatment option for patients in the future.