Feb. 25, 2026
According to a 2025 systematic review published in Reviews in the Neurosciences, PBM exerts its neuroprotective effects through the following pathways:
Enhanced Energy Metabolism: Absorbed by cytochrome c oxidase (CCO) in neuronal mitochondria, increasing ATP synthesis.
Increased Cerebral Blood Flow (CBF).
Regulation of Oxidative Stress.
Anti-inflammatory Effects.
Neuroprotection and Regeneration.Enhanced Synaptic Plasticity.
Regulation of Resting-State Brain Networks.
·
A 2025 workshop hosted by the US National Institute on Aging (NIA) further confirmed that PBM acts by stimulating mitochondrial CCO, modulating cell membrane transporters and receptors, and activating transforming growth factor-beta 1 (TGF-β1), among other mechanisms.
Disease | 660nm | 810nm | 1065nm |
Alzheimer‘s Disease | Antioxidant, reduces Aβ toxicity | Induces anti-Aβ neurons, modulates neuroinflammation | Heat shock protein pathway (theoretical) |
Stroke | Adjunctive therapy (limited research) | Neuroprotection, promotes functional recovery | Deep vasodilation, improves blood flow |
Parkinson’s Disease | Peripheral adjunct | Protects dopaminergic neurons | Deep brain modulation (theoretical) |
Traumatic Brain Injury | Improves sleep (combined with 830nm) | Increases CBF, improves executive function | Deep tissue repair (theoretical) |
Brain Tumors | Contraindicated | Contraindicated | Contraindicated |
Brain Atrophy | Adjunctive role | Promotes neurogenesis, reduces apoptosis | Nutrient supply to deep brain regions |
Cerebral Arteriosclerosis | Limited effect | Improves endothelial function | Preferred: Vasodilation, increases blood flow |
Therapeutic Principles:
1.
Induction of Anti-Aβ Neurons:
A 2026 study published in the Journal of Alzheimer’s Disease showed that treating hippocampal neural stem cells with pulsed 808nm near-infrared laser could generate neurons resistant to the toxicity of amyloid-beta oligomers (AβO) . Specific mechanisms include:
2.Reduced binding capacity of AβO to neurons.
Protection of mitochondria from AβO-induced toxicity.
Increased expression of genes related to autophagy and protein homeostasis.
Regulation of Neuroinflammation and Apoptosis-Related Genes:
A 2025 study in PLoS ONE treated mice with transcranial 808nm PBM (1 hour daily for 30 days). Whole RNA sequencing revealed:
1,005 genes showed transcriptional changes in the hippocampus, and 1,482 genes changed in the cortex.
Regulation of genes related to oxidative stress: NF-κBIα, JUN, JUND, PKC.
Regulation of genes related to inflammation: DOCK4/6, IL-1RAPL1, TNFαIP6.
Regulation of genes related to apoptosis: CASP3, TNFαIP6, AKT3, CDKN1A.
Regulation of major AD risk genes: BACE1, BACE2, PSEN2, APH1B, STAT3, etc.
Significant reduction in APP concentration.
A 2023 study in PLoS ONE demonstrated that both 660nm and 810nm LED (3 J/cm²) protected neurons from Aβ1-42-induced neurotoxicity by:
Reducing intracellular reactive oxygen species (ROS) generation.
Decreasing Ca²⁺ influx.
Restoring neurite outgrowth.
Exhibiting a biphasic dose response, with 3 J/cm² being most effective.
Research indexed in the NIH database indicates that light in the 1040-1267nm range (including 1065nm) can act on AD models by:
Reducing Aβ oligomers.
Inducing heat shock protein expression.
Can be used in continuous wave or pulsed modes (10/40/600Hz).
FDA-Registered Clinical Trial: New York University Langone Medical Center is conducting an FDA-registered clinical trial (NCT06956404) evaluating 808nm laser therapy in older adults with chronic TBI:
Intervention: 808nm continuous laser applied to the forehead, approx. 12 minutes per session, 3 times weekly for 6 weeks.
Primary Endpoints: Change in prefrontal cerebral blood flow (CBF) and improvement in executive function.
Completion expected in 2028; represents a top-tier clinical evidence source in the TBI field.
Neuroprotective Mechanisms:
A 2025 review in Brain Research systematically outlines PBM‘s neuroprotective mechanisms in stroke:
Activation of key chromophores: cytochrome c oxidase, calcium channels.
Consideration of water as a significant chromophore, potentially enhancing therapeutic effects.
Combination treatment strategies: targeting both the brain and skeletal muscle may be more effective for improving post-stroke hemiplegia.
Although 755nm is not one of the wavelengths inquired about, a 2025 study in Cyborg and Bionic Systems revealed novel mechanisms of PBM in stroke:
755nm light accelerates molecular transport in the brain’s extracellular space (ECS) and interstitial fluid drainage.
Promotes clearance of pro-inflammatory cytokines.
Reduces pathological protein deposition.
Achieves these effects by modulating the expression and polarization of aquaporin-4 (AQP4).
Ultimately reduces infarct volume and improves neurocognitive function.
Based on the deeper tissue penetration of 1065nm, it could theoretically be used to improve deep blood perfusion in ischemic areas, though more direct evidence is needed.
