Alzheimer’s disease (AD) remains one of the most challenging and devastating neurodegenerative conditions affecting millions worldwide. Characterized by progressive cognitive decline, memory loss, and behavioral changes, AD not only affects the individual but also imposes a significant burden on caregivers and healthcare systems. Despite extensive research, effective treatments for AD are still elusive. However, a promising avenue of investigation has emerged in recent years – brain photobiomodulation (PBM).

Brain PBM, also known as transcranial light therapy or low-level light therapy, involves the non-invasive application of high-power density NIR light energy through the scalp, to the brain, stimulating cellular function and promoting tissue repair. While initially explored for its potential in wound healing and pain management, researchers are increasingly investigating its therapeutic effects on neurological disorders, including AD.

Understanding Alzheimer’s Disease

Before delving into the potential of PBM in AD, it’s crucial to grasp the underlying mechanisms of the disease. AD is characterized by the accumulation of beta-amyloid plaques and tau protein tangles in the brain, leading to neuronal dysfunction and eventual cell death. Additionally, oxidative stress, inflammation, and impaired mitochondrial function contribute to the progression of the disease.

The mechanisms of brain photobiomodulation

How Photobiomodulation Works against Alzheimer’s Disease

When near-infrared light energy penetrates the scalp and skull, reaching neuronal tissue – it is absorbed by mitochondria, enhancing cellular metabolism, increasing ATP production, and reducing oxidative stress and inflammation.

The therapeutic effects of PBM in AD are thought to stem from its ability to modulate various cellular processes implicated in the pathogenesis of the disease.

One key mechanism of PBM against AD is the stimulation of mitochondrial function. Mitochondrial dysfunction is a hallmark of AD and is believed to contribute to neuronal degeneration. By enhancing mitochondrial activity, PBM may help improve cellular energy production and mitigate oxidative stress, thereby protecting neurons from damage.

Besides that, by reducing oxidative stress, PBM may mitigate neuronal damage and promote cellular survival. Oxidative stress arises from an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify them, leading to cellular damage and dysfunction. PBM has been shown to enhance the activity of antioxidant enzymes, such as superoxide dismutase (SOD) and catalase, while simultaneously reducing the production of ROS. This dual effect helps to restore redox balance within neurons, thereby protecting them from oxidative damage and promoting cellular survival. By targeting oxidative stress, PBM may offer neuroprotective benefits in AD, potentially slowing disease progression and preserving cognitive function.

PBM has also been shown to modulate inflammatory pathways, potentially attenuating neuroinflammation, which is another hallmark of AD. This anti-inflammatory effect of PBM holds significant implications for the treatment of AD, as chronic neuroinflammation contributes to neuronal damage and cognitive decline.

Furthermore, PBM has been shown to promote neurogenesis and synaptogenesis, processes essential for maintaining cognitive function and synaptic plasticity. By stimulating the growth of new neurons and strengthening synaptic connections, PBM may help counteract the neuronal loss and synaptic disruption characteristic of AD.

How Does NIR Light Energy Reach the Brain?

In order to deliver NIR energy to the brain through the skull, scalp and hair to trigger photobiomodulation, this requires 3 important factors:

Clinical Evidence of PBM and Alzheimer’s Disease

Several preclinical studies have demonstrated the beneficial effects of PBM in animal models of AD. For instance, a study published in Neurobiology of Aging by De Taboada et al. (2011) showed that transcranial PBM reduced beta-amyloid plaques and improved memory in a mouse model of AD.[1] Similarly, another study by Yang et al. (2018) in Neurophotonics reported that PBM decreased tau protein hyperphosphorylation and alleviated cognitive deficits in AD mice.[2]

Clinical Research with the Vielight Neuro Gamma

The Vielight Neuro Gamma

Clinical evidence with the Vielight Neuro suggests that PBM may offer therapeutic benefits in human patients with AD.

A pilot study conducted by Saltmarche et al. (2017) with the Vielight Neuro and published in Journal of Alzheimer’s Disease found that transcranial PBM improved cognitive function and activities of daily living in patients with mild-to-moderate AD.

In 2019, Dr. Linda Chao, a professor in the Departments of Radiology, Biomedical Imaging and Psychiatry at the University of California, verified our 2015 dementia pilot trial with her own independent brain photobiomodulation dementia study with the Vielight Neuro Gamma on participants with dementia.[2]

Eight participants diagnosed with dementia were randomized to 12 weeks of usual care or home photobiomodulation(PBM) treatments. The PBM treatments were administered at home with the Vielight Neuro Gamma, a brain photobiomodulation device that emits 100 mW/cm2 of power density at 810nm and 40hz.

Several types of assessments were used:

  • Alzheimer’s Disease Assessment Scale-cognitive subscale and the Neuropsychiatric Inventory at baseline and 6 and 12 weeks
  • Magnetic resonance imaging (MRI) and resting-state functional MRI at baseline and 12 weeks.
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Figure 1. ADAS-cog (A) and NPI-FS (B) scores in the PBM (blue line) and UC (red line) groups by time. Lower scores on both measures indicate better function.

After 12 weeks, there were improvements in ADAS-cog and in the NPI.

A summary measure of the individual domain scores: higher NPI-FS scores reflect more severe/more frequent dementia-related behavior.

In this study, the PBM group improved an average of -12.3 points on the NPI-FS after 6 weeks and -22.8 points after 12 weeks of treatments.

By comparison, previous pharmacological trials of donepezil reported no difference from placebo on behavioral symptoms measured by the NPI and no difference on quality of life.

Importantly, there were no adverse effects associated with the PBM treatments in this or Saltmarche et al.’s study. In contrast, many of the Food and Drug Administration approved pharmacological treatments for dementia have been associated with substantial side effect burden, such as diarrhea, vomiting, nausea, and fatigue.

Figure 2 Increased cerebral perfusion with the Vielight Neuro Gamma

The third finding of this study is that cerebral perfusion (CBF) increased after 12 weeks in the PBM group compared to the UC group. This finding is consistent with previous reports of PBM-related increases in local CBF, oxygen consumption, total hemoglobin, a proxy for increased rCBF, rCBF, and increased oxygenated/decreased deoxygenated hemoglobin concentrations.

Interestingly, the PBM-related increases in perfusion were most prominent in the parietal ROIs. This may relate to the fact that the Vielight Neuro Gamma used in this study had three transcranial LED clusters over the parietal lobe and only one transcranial LED cluster over the frontal lobe. This finding may also be explained by the report that NIR light penetrates more deeply through the parietal lobe compared to the frontal lobe due to the higher power density of the rear transcranial LED modules .

Connectivity changes in the DMN have been described in populations at risk for AD as well as in patients with AD. Because decreased DMN connectivity is a common finding in resting-state connectivity studies of AD, it is significant that there was increased functional connectivity between the PCC and the LP nodes of the DMN in the PBM group after 12 weeks compared to the UC group.

There have been reports of increased functional connectivity in the DMN after pharmacological treatments in mild-to-moderate AD patients. There have also been studies that reported changes in functional connectivity after nonpharmacological intervention in patients with MCI. To our knowledge, this is the first report of functional connectivity changes in dementia patients after a nonpharmacological intervention.

Neuro RX Gamma – Phase 3 Clinical Trial

We are running a Phase 3 Alzheimer’s Clinical Trial to test the efficacy of brain photobiomodulation via the Vielight Neuro RX Gamma (Neuro Gamma) for FDA approval. This would add to our roster of Health Canada Medical Device license for the acceleration of the recovery of upper respiratory symptoms in viral infections, such as COVID-19 with the RX-Plus (X-Plus 4).


Alzheimer’s disease poses a significant challenge to global health, necessitating innovative approaches for treatment and management. Brain photobiomodulation represents a promising therapeutic modality that harnesses the power of light to stimulate cellular function and promote neuroprotection. While further research is warranted, the emerging evidence suggests that PBM may offer hope for individuals living with AD and their families.

In conclusion, brain photobiomodulation holds tremendous potential as a non-invasive, safe, and effective intervention for Alzheimer’s disease. By addressing underlying pathological mechanisms and promoting neuronal health, PBM may usher in a new era of treatment for this devastating condition.


  1. De Taboada L, et al. (2011). Transcranial laser therapy attenuates amyloid-β peptide neuropathology in amyloid-β protein precursor transgenic mice. Neurobiology of Aging, 32(1), 25-28.
  2. Yang X, et al. (2018). Transcranial low-level laser therapy improves cognitive deficits and inhibits microglial activation after controlled cortical impact in mice. Neurophotonics, 5(1), 015001.
  3. Saltmarche AE, et al. (2017). Significant Improvement in Cognition in Mild to Moderately Severe Dementia Cases Treated with Transcranial Plus Intranasal Photobiomodulation: Case Series Report. Journal of Alzheimer’s Disease, 60(2), 1-13.
  4. Vemuri P, Jones DT, Jack CR, Jr. Resting state functional MRI in Alzheimer’s Disease. Alzheimers Res Ther 2012;4:2
  5. Sole-Padulles C, Bartres-Faz D, Llado A, et al. Donepezil treatment stabilizes functional connectivity during resting state and brain activity during memory encoding in Alzheimer’s disease. J Clin Psychopharmacol 2013;33:199–205.
  6. Goveas JS, Xie C, Ward BD, Wu Z, Li W, Franczak M. Recovery of hippocampal network connectivity correlates with cognitive improvement in mild Alzheimer’s disease patients treated with donepezil assessed by resting-state fMRi. J Magn Reson Imaging 2011;34:764–773.
  7. Li W, Antuono PG, Xie C, et al. Changes in regional cerebral blood flow and functional connectivity in the cholinergic pathway associated with cognitive performance in subjects with mild Alzheimer’s disease after 12-week donepezil treatment. Neuroimage 2012;60:1083–1091.