Abstract:

Alzheimer’s disease (AD) is a major public health problem all over the world. Therapeutic strategies have been explored for several decades, but no curative treatment has been developed (1). Although the FDA has recently approved lecanemab (Leqembi) and donanemab (Kisunla) for treating cognitive decline in early Alzheimer’s disease, their efficacy is modest, with potential side effects like amyloid-related imaging abnormalities (ARIA), and their long-term impact on disease progression remains uncertain, particularly in advanced stages (2, 3). However, these drugs represent a significant advancement by objectively reducing amyloid beta (Aβ) markers, which purportedly slow disease progression in patients with early-stage AD, marking an important first step toward more effective therapies.

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Photobiomodulation therapy (PBMT) is a rapidly growing approach to the healing, stimulation, protection, and regeneration of many human organs and tissue types. PBMT started in the 1960s as low-level laser therapy for wound healing, but since then the introduction of light-emitting diodes (LEDs) has dramatically increased the number of applications and reports of positive results. PBMT generally uses red (620–700 nm) and/or near-infrared (780–1270 nm) wavelengths of light at an intensity that causes no tissue heating, and its activity is based on well-established biological and cellular mechanisms (de Freitas and Hamblin, 2016). While laser therapists continue to use various types of laser in their office practice, LEDs are ideally suited for home use devices because they are completely safe and without any known significant adverse effects. Among the various body parts on which PBMT has been shown to exert beneficial effects, the brain stands out as perhaps the most promising overall. PBMT has been shown to reduce neuroinflammation, while increasing mitochondrial function, oxygen consumption, and blood flow within the brain (Hamblin, 2016). Moreover, PBMT can stimulate the processes of synaptogenesis, neurogenesis, and neuroplasticity thus helping the brain to heal itself. PBMT has neuroprotective activity and can prevent brain damage in the acute phase after traumatic brain injury or stroke, because it inhibits apoptosis and upregulates the expression of anti-apoptotic proteins, as well as improving brain metabolism and oxygenation. In the chronic phase, PBMT can improve memory, cognitive function, mood, and sleep quality. In degenerative brain disorders (dementia, Alzheimer’s disease, and Parkinson’s disease), PBMT can improve motor, cognitive and social functioning (at least for some time). In a range of psychiatric disorders (depression, anxiety, autism spectrum disorder, and opioid addiction), PBMT can lead to significant improvements (Salehpour et al., 2018). This perspective will outline the mechanisms of action of PBMT on cells and tissues, and summarize the wide range of current applications to the brain, while proposing some new directions in psychiatry.

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Abstract

Background: Transcranial photobiomodulation (tPBM) has been studied for over a decade as a possible cognitive intervention.

Objective: To evaluate the effect of tPBM for enhancing human cognitive function in healthy adults and remediating impaired cognitive function in adults with cognitive disorders.

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Abstract

Dementia is a complex syndrome with various presentations depending on the underlying pathologies. Low emission of transcranial near-infrared (tNIR) light can reach human brain parenchyma and be beneficial to a number of neurological and neurodegenerative disorders. We hereby examined the safety and potential therapeutic benefits of tNIR light stimulations in the treatment of dementia. Patients of mild to moderate dementia were randomized into active and sham treatment groups at 2:1 ratio. Active treatment consisted of low power tNIR light stimulations with an active photobiomodulation for 6 min twice daily during 8 consequent weeks. Sham treatment consisted of same treatment routine with a sham device. Neuropsychological battery was obtained before and after treatment. Analysis of variance (ANOVA) was used to analyze outcomes. Sixty subjects were enrolled. Fifty-seven subjects completed the study and had not reported health or adverse side effects during or after the treatment. Three subjects dropped out from trial for health issues unrelated to use of tNIR light treatment. Treatment with active device resulted in improvements of cognitive functions and changes were: an average increase of MMSE by 4.8 points; Logical Memory Tests I and II by ~3.0 points; Trail Making Tests A and B by ~24%; Boston Naming Test by ~9%; improvement of both Auditory Verbal Learning Tests in all subtest categories and overall time of performance. Many patients reported improved sleep after ~7 days of treatment. Caregivers noted that patients had less anxiety, improved mood, energy, and positive daily routine after ~14-21 days of treatment. The tNIR light treatments demonstrated safety and positive cognitive improvements in patients with dementia. Developed treatment protocol can be conveniently used at home. This study suggests that additional dementia treatment trials are warranted with a focus on mitigating caregivers’ burden with tNIR light treatment of dementia patients.

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