Can Light Therapy Help Alzheimer's? What the Science Says About tPBM

Hi Phoenix friend,

The following is a guest post by Nicole Greig, from Neuronic.
The Phoenix community has recently published the results of our Neuronic Study where 55 APOE4 carriers used red light therapy for 4 months.
If you’d like to get the device we used: Get $100 off the Neuronic LIGHT device, with the code PHOENIX

We had very exciting results, and I’d encourage you to use the device for yourself, and track it with Phoenix. Neuronic offers a 90-day money-back guarantee, so if it doesn’t work for you, you can simply just return the device.

But without further ado, here’s Nicole taking over:

What Is Alzheimer's Disease?

Alzheimer's disease is the most common form of dementia, affecting millions of people worldwide. It is a progressive neurodegenerative condition, meaning it gradually worsens over time as brain cells lose function and die. While it is most commonly diagnosed in people over 65, it is not a normal part of aging; it is a disease with specific biological causes that researchers are still working to fully understand.

The earliest signs are often subtle: forgetting recent conversations, misplacing items, or struggling to find words. Over time, Alzheimer's erodes memory, reasoning, language, and the ability to carry out daily tasks, eventually requiring full-time care.

What Happens Inside the Brain?

At the biological level, Alzheimer's begins when the brain starts producing toxic amyloid-beta fragments that build up into sticky plaques - one of the disease's defining features. This triggers a damaging cycle: mitochondrial dysfunction drives more amyloid production, and that excess amyloid causes further mitochondrial damage. Meanwhile, tau proteins inside neurons begin to misfold and tangle, breaking down the internal structure that keeps brain cells alive and communicating.

Together, these processes spark chronic neuroinflammation and oxidative stress, gradually destroying the synaptic connections that allow neurons to talk to one another. It is this slow unraveling of neural networks that leads to the memory loss and cognitive decline Alzheimer's is known for.

Who is at Risk for Alzheimer’s Disease? The Role of the APOE4 Gene 

APOE4 is a variant of the apolipoprotein E gene, which plays a key role in how the brain manages cholesterol and fat transport (Liu et al., 2013). Not everyone who develops Alzheimer's carries this variant, but carrying it significantly shifts the odds. Compared to people without it, those with one copy face an 3 to 7 times increased risk of developing Alzheimer's disease, and those who carry two copies face 12 times the risk (Pires & Rego, 2023). The APOE4 variant disrupts normal cholesterol regulation in the brain, which can impair synaptogenesis and myelination, and may contribute to the formation of toxic protein aggregates like amyloid-beta plaques (Liu et al., 2013).

Importantly, carrying this gene is not a diagnosis, but it is a risk factor. Many APOE4 carriers never develop Alzheimer's, and understanding your genetic risk is one of the most powerful tools you have for taking an active, informed approach to brain health.

A Promising Approach to Alzheimer’s Disease: Transcranial Photobiomodulation

If you've spent any time researching ways to support brain health, you may have come across the term transcranial photobiomodulation, often shortened to tPBM, and sometimes called low-level laser therapy (LLLT) or near-infrared light therapy. 

At its core, it's a simple idea: shining specific wavelengths of red or near-infrared light through the scalp and skull to reach brain tissue underneath. First discovered by Endre Mester and colleagues in 1968, tPBM operates within wavelengths of 600 to 1100 nanometers - a range scientists call the "optical window" because it passes through skin and bone without being absorbed before reaching its target. Unlike UV light or X-rays, it doesn't damage tissue or carry radiation risk.

The optical window of PBM. (Image source: Santos et al., 2019).

What makes tPBM particularly relevant for Alzheimer's risk is where that light goes once it enters the body. Studies using human cadaver heads found that light in the 808 nanometer range can penetrate 40–50 millimeters into brain tissue, with roughly 1–2% of light delivered to the scalp ultimately reaching the cortical surface (Tedford et al., 2015). That might sound like a small amount - but as you'll see in the sections ahead, even a modest dose of light energy reaching brain cells appears to be enough to influence the mitochondrial processes that break down in Alzheimer's disease. Devices range from clinical lasers used in research settings to wearable LED helmets designed for home use.

How Transcranial Photobiomodulation Works: The Mechanisms

1. The Light Reaches the Brain

tPBM uses specific wavelengths of near-infrared light - generally between about 800 nm and 1070 nm - that are able to pass through hair, scalp, and skull to reach brain tissue. Many studies focus especially on the prefrontal cortex, the area involved in focus, mood, decision-making, and emotional regulation. The light isn't there to "zap" neurons. It's there to support, restore, and regulate naturally occurring cellular processes.

2. The Mitochondria (Your Brain's "Power Plants") Absorb the Light

Inside each brain cell are mitochondria, colloquially known as the "powerhouse of the cell" - tiny structures responsible for making energy. One key mitochondrial enzyme, called cytochrome c oxidase, happens to be sensitive to near-infrared light. When this enzyme absorbs light, it becomes more efficient at doing its job. In simple terms: your brain cells get better at making energy in the form of adenosine triphosphate, or ATP.

3. A Roadblock Gets Cleared - Nitric Oxide

Under stress or inflammation, a molecule called nitric oxide can bind to cytochrome c oxidase in the same spot that oxygen needs to occupy in order to trigger ATP production - essentially blocking the process. Light helps knock that nitric oxide loose. Once it's displaced, oxygen can bind again and energy production can resume normally.

The effects of PBM on the electron transport chain (Image Source: Scientific Research).

4. Energy Production Turns Back On

With oxygen flowing properly, mitochondria are able to more efficiently execute their full energy-making process, allowing cells to produce more ATP - the fuel the brain uses for virtually everything, from firing signals to repairing itself.

5. More ATP Means a Brain That Has the Energy to Function

When ATP levels increase, neurons are better equipped to communicate with each other, repair and maintain connections, and support learning and adaptation. This is why people often associate tPBM with clearer thinking, reduced brain fog, and improved mental stamina.

6. A Small, Protective Stress Signal Is Triggered

As energy production ramps up, there's a mild increase in reactive oxygen species, or ROS. While that might sound concerning, this small increase actually acts as a signal that prompts cells to activate their own protective and adaptive pathways. In moderation, this process helps cells become more resilient over time.

7. Blood Flow Improves

tPBM also supports better cerebral blood flow, in part because nitric oxide - now released from the enzyme - helps blood vessels relax and widen. This means more oxygen and nutrients are delivered to brain tissue, while waste products are cleared more efficiently. Better circulation supports overall brain health and recovery.

8. Inflammation Calms Down

Chronic inflammation can interfere with how well neurons communicate. Research shows that photobiomodulation helps reduce inflammatory signaling and oxidative stress, creating a more supportive environment for brain function. With less background "noise," the brain can operate more smoothly.

9. The Brain Becomes More Adaptable

When you combine better energy availability, improved blood flow, lower inflammation, and healthier mitochondria, you create ideal conditions for neuroplasticity - the brain's ability to adapt, rewire, and recover. This is where people may notice real-world benefits like improved focus, sharper memory, better mood regulation, or faster recovery after stress or cognitive fatigue.

What Does tPBM Do to Amyloid Plaques and Tau?

Two of the most defining features of Alzheimer's disease - amyloid-beta plaques and tau tangles - are not just markers of damage. They are active drivers of the cognitive decline the disease is known for. So one of the most important questions researchers are asking is whether tPBM can do anything to slow or reverse their accumulation. The evidence so far suggests it can, through several interconnected pathways.

PBM has been shown to reduce the formation of both tau tangles and amyloid-beta plaques, alongside reducing reactive oxygen species and inflammation - all of which are key contributors to neurodegeneration (Wang et al., 2024). On the amyloid side, the mechanism appears to work at least in part through the cell's own cleanup systems. Previous studies have shown that PBM reduces amyloid-beta load primarily by enhancing the clearance capabilities of glial cells - the brain's immune and support cells - while more recent research suggests PBM may also directly reduce amyloid formation within neurons themselves, independent of glial cell involvement (Ramanishankar et al., 2024).

Additional findings suggest that PBM may modulate brain activity at gamma frequencies, which could activate peptides that upregulate glymphatic activity and further enhance amyloid clearance - essentially helping the brain's waste removal system work more efficiently overnight (Valverde et al., 2023). Research on the tau protein and pulse frequency shows that PBM at 10 Hz may induce tubulin depolymerization, potentially destabilizing the misfolded proteins associated with neurofibrillary tangles, while 40 Hz PBM may then help stabilize microtubular structures and support neuronal network integrity (Lim et al., 2025). Taken together, tPBM appears to work on Alzheimer's pathology not through a single targeted mechanism, but through a coordinated set of cellular and immune processes that address both hallmark pathologies simultaneously.

Human Studies: What the Research Says

In human trials, the landmark early study by Saltmarche et al. (2017) reported measurable improvements on the MMSE and ADAS-Cog cognitive scales in dementia patients after 12 weeks of transcranial PBM. Caregivers also noted that patients slept better, had fewer angry outbursts, and experienced less anxiety - though gains were not sustained after treatment ended, suggesting tPBM may need to be used as an ongoing intervention rather than a fixed course.

A second notable human study comes from Nizamutdinov et al. (2021), who enrolled 60 dementia patients in a sham-controlled trial of transcranial and ocular near-infrared light therapy. Participants received continuous 1,060–1,080 nm light for six-minute sessions, twice daily over 12 weeks, with results showing statistically significant improvements in MMSE and cognitive memory scores compared to the sham group - making it one of the larger and more rigorously controlled human studies conducted to date. Importantly, the trial demonstrated not only measurable cognitive gains but also a favorable safety profile across all participants, reinforcing that tPBM is well tolerated even with extended daily use (Nizamutdinov et al., 2021).

The Future of Photobiomodulation in Alzheimer's Treatment

The science of tPBM for Alzheimer's is advancing rapidly, and what once looked like a speculative therapy is increasingly being taken seriously by academic medical centers worldwide. Several promising directions are emerging - including the use of specific pulse frequencies to restore gamma brain rhythms disrupted in early Alzheimer's, EEG-guided personalization that tailors treatment to an individual's unique brain activity patterns, and the integration of tPBM alongside pharmaceutical therapies as part of a broader combination approach. 

For APOE4 carriers in particular, tPBM's non-invasive nature and favorable safety profile make it a compelling area to watch. While it is not yet an approved or standardized treatment for Alzheimer's disease, the depth and quality of research is growing around it, from transgenic animal models to brain imaging to randomized controlled trials. 

Get $100 off the Neuronic LIGHT device, with the code PHOENIX

References:

Lim, L., Staelens, M. A., Truglia, B., Lazzari, D. D., Gregorio, E. D., Shankar, K., Liburd, J., Hosseinkhah, N., Karimpoor, M., & Tuszynski, J. A. (2025). Beyond Gamma: Synergistic Potential of 10 Hz Alpha and 40 Hz Gamma Photobiomodulation in Alzheimer's Disease Treatment. Alzheimer's & Dementia, 21(Suppl 1), e105314. https://doi.org/10.1002/alz70855_105314

Liu, C. C., Liu, C. C., Kanekiyo, T., Xu, H., & Bu, G. (2013). Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy. Nature reviews. Neurology, 9(2), 106–118. https://doi.org/10.1038/nrneurol.2012.263

Nizamutdinov, D., Qi, X., Berman, M. H., Dougal, G., Dayawansa, S., Wu, E., Yi, S. S., Stevens, A. B., & Huang, J. H. (2021). Transcranial near infrared light stimulations improve cognition in patients with dementia. Aging and Disease, 12(3), 954–963. https://doi.org/10.14336/AD.2021.0229

Pires, M., & Rego, A. C. (2023). Apoe4 and Alzheimer's Disease Pathogenesis-Mitochondrial Deregulation and Targeted Therapeutic Strategies. International journal of molecular sciences, 24(1), 778. https://doi.org/10.3390/ijms24010778

Ramanishankar, A., S, A. S., Begum, R. F., Jayasankar, N., Nayeem, A., Prajapati, B. G., & Nirenjen, S. (2024). Unleashing light's healing power: an overview of photobiomodulation for Alzheimer's treatment. Future science OA, 10(1), FSO922. https://doi.org/10.2144/fsoa-2023-0155

Saltmarche, A. E., Naeser, M. A., Ho, K. F., Hamblin, M. R., & Lim, L. (2017). Significant improvement in cognition in mild to moderately severe dementia cases treated with transcranial plus intranasal photobiomodulation: Case series report. Photomedicine and Laser Surgery, 35(8), 432–441. https://doi.org/10.1089/pho.2016.4227

Santos, E. A. B., Lucena, R. J. R. S., Lima, E. G., Lins, L. T., & Rodrigues, M. A. B. (2019). Low-cost functional near infrared spectroscopy (fNIRS) applied on brain-computer interfaces (BCIs). In R. Costa-Felix et al. (Eds.), XXVI Brazilian Congress on Biomedical Engineering: IFMBE Proceedings (Vol. 70/1, pp. 495-500). Springer. https://doi.org/10.1007/978-981-13-2119-1_76

Tedford, C. E., DeLapp, S., Jacques, S., & Anders, J. (2015). Quantitative analysis of transcranial and intraparenchymal light penetration in human cadaver brain tissue. Lasers in Surgery and Medicine, 47(4), 312–322. https://doi.org/10.1002/lsm.22343

Valverde, A., Hamilton, C., Moro, C., Billeres, M., Magistretti, P., & Mitrofanis, J. (2023). Lights at night: does photobiomodulation improve sleep?. Neural regeneration research, 18(3), 474–477. https://doi.org/10.4103/1673-5374.350191

Wang, M., Dinarvand, D., Chan, C. T. Y., Bragin, A., & Li, L. (2024). Photobiomodulation as a Potential Treatment for Alzheimer’s Disease: A Review Paper. Brain Sciences, 14(11), 1064. https://doi.org/10.3390/brainsci14111064