Conclusion

The Vielight Neuro VieLED architecture is deceptively simple: by leveraging tissue optics, it yields an effectively full‑transcranial energy footprint with a purposeful DMN bias. The intranasal channel completes the map by accessing ventral forebrain across the porous cribriform plate, creating a complementary dorsal‑to‑ventral pathway. The calvaria‑based visualizations make the physics tangible—five LEDs, one brain‑wide footprint, with DMN‑centered emphasis by design.

Investigating Photobiomodulation as a Cognitive Intervention for Repetitive Head Acceleration Events

This n=44 TBI clinical study conducted by researchers from the University of Utah, Brigham Young University, and affiliated institutions explored the potential of transcranial and intranasal photobiomodulation (PBM) to improve cognitive function in individuals with a history of repetitive head acceleration events (RHAEs).

This builds on the previous n=43 published TBI clinical study by the University of Utah.

These events, often experienced in contact sports and military contexts, may not cause immediate concussions but are known to contribute cumulatively to cognitive decline and increased risk of neurodegeneration over time.

READ THE FULL PUBLISHED STUDY HERE | Published Study Link

“Football almost killed me… But Vielight saved my life.” — Dr. Larry Carr.

Study Objective

The goal was to assess whether near-infrared PBM therapy using an 810 nm LED device could produce measurable improvements in cognitive performance. This approach was motivated by the need for effective, non-invasive treatments targeting the underlying neural mechanisms affected by RHAEs.

Participant Profile

• N = 44 (90% male; mean age = 46)

• History of RHAEs averaging 12.4 years

• Participants were excluded if they had known neurological diseases or major psychiatric disorders

Intervention Protocol

Each participant received a Vielight Neuro Gamma (v3) device, which delivers near-infrared light to cortical and subcortical brain regions through both transcranial and intranasal routes:

• LEDs targeted the dorsomedial prefrontal cortex, lateral parietal lobes, and midline precuneus

• An intranasal LED directed light toward orbitofrontal and olfactory-associated brain structures

• Sessions lasted 20 minutes and were conducted every other day over 8–10 weeks (mean = 29 sessions)

Cognitive Assessments

A comprehensive battery of validated neuropsychological tests was administered before and after the intervention, measuring domains including:

• Verbal learning and memory (CVLT-3)

• Executive function (D-KEFS)

• Sustained attention (CPT-3)

• Global cognition (NIH Toolbox Cognition Battery)

Key Findings

University of Utah diffusion-MRI (DTI) tractography maps show decreased inflammation-related diffusion markers with Vielight Neuro versus placebo

Group-level improvements were statistically significant across several domains:

• Verbal memory: Learning and delayed recall improved (Cohen’s d = 0.49–0.62)

• Executive function: Inhibition and cognitive switching improved (d = 0.54–0.67)

• Attention: Enhanced sustained attention and fewer omission/commission errors (d = -0.34 to -0.67)

• Fluid cognition and processing speed: Moderate-to-large effect sizes observed (d = 0.45–0.94)

Crystallized abilities such as vocabulary and reading remained stable, supporting the specificity of PBM’s effect on vulnerable cognitive functions.

Individual-Level Analysis

Reliable Change Index (RCI) calculations revealed:

• 14–36% of participants showed reliable improvement in select domains

• Improvements were most common in attention, memory, and processing speed

• Very few participants demonstrated any reliable cognitive decline

Proposed Mechanism

PBM is believed to act via mitochondrial cytochrome c oxidase, leading to increased ATP production, nitric oxide release, anti-inflammatory effects, and neuroplastic adaptations. These mechanisms may underlie the observed cognitive benefits.

Conclusion

This study provides preliminary evidence that PBM may offer cognitive benefits for individuals exposed to repetitive neurotrauma. The observed improvements, particularly in fluid cognition and memory, suggest PBM could be a promising candidate for non-pharmacological neurorehabilitation. While further research is needed to validate these findings, this study marks an important step toward establishing PBM as a viable intervention for cognitive impairment following RHAEs.

Read the full Alzheimer’s Disease published study with the Vielight Neuro here: Link

Introduction

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:

• NIR light energy wavelengths: 810nm to 1100nm
  – optimal penetrance based on the body’s optical window.
• A form factor that bypasses hair and maximizes contact with the scalp
  – hair absorbs light energy.
  – light energy becomes weaker from distance, according to the inverse square law of light.
• Sufficiently high power density/irradiance: 100+ mW/cm²
  – sufficient power density/irradiance is required for light energy to penetrate the scalp and bone.

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.

Results:

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).

Conclusion

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.

References:

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.

Parkinson’s disease (PD) is a debilitating neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta, located in the midbrain section, which controls movement. This leads to motor and non-motor symptoms.

Brain photobiomodulation (PBM) has emerged as a promising non-invasive approach for neuroprotection in PD. This article reviews the underlying mechanisms of PBM and its potential application in PD therapy, based on preclinical and clinical evidence.

Introduction

Parkinson’s disease (PD) is the second most common neurodegenerative disorder, the first being Alzheimer’s disease. While the direct causes of PD remains unknown, mitochondrial dysfunction, oxidative stress, and neuroinflammation are thought to contribute to the progressive loss of dopaminergic neurons in the substantia nigra. Current treatments provide symptomatic relief but do not halt disease progression.

Brain photobiomodulation (PBM) offers a novel therapeutic strategy by harnessing the well-researchedneuroprotective properties of NIR light energy to mitigate pathological processes implicated in PD.

Clinical Research for Parkinsons Study the Vielight Neuro Gamma

The Vielight Neuro Gamma

In an independent Parkinson’s study by Dr. Ann Liebert et al, from the University of Sydney, the Vielight Neuro Gamma was utilized for transcranial-intranasal brain photobiomodulation and produced statistically significant clinical results.

Methods: Twelve participants diagnosed with idiopathic Parkinson’s disease (PD) were enlisted for the study. Random selection was employed, with six participants assigned to undergo 12 weeks of transcranial, intranasal, neck, and abdominal photobiomodulation (PBM) treatment. The remaining six participants were placed on a waitlist for 14 weeks before initiating the same treatment. Following the 12-week treatment period, all participants were provided with PBM devices for continued home treatment. Assessments of mobility, fine motor skills, balance, and cognition were conducted at baseline, after 4 weeks of treatment, after 12 weeks of treatment, and at the conclusion of the home treatment period. Treatment effectiveness was evaluated using the Wilcoxon Signed Ranks test with a significance level set at 5%.

Results: Significant improvements (p < 0.05) in measures of mobility, cognition, dynamic balance, and fine motor skills were observed with 12 weeks of PBM treatment, persisting for up to one year. Many individual improvements exceeded the threshold deemed clinically meaningful for participants, with variations in the extent of improvement. Notably, improvements were sustained for up to one year with continued home treatment, indicating a sustained treatment effect. A minor Hawthorne Effect was observed, which was below the treatment effect, and no adverse side effects of the treatment were noted.

Figure 3 – Heatmap of Parkinsons Photobiomodulation Clinical Results – University of Sydney

PBM emerged as a safe and potentially effective intervention for addressing various clinical manifestations of PD. The observed improvements were sustained as long as the treatment was continued, even in a neurodegenerative condition where deterioration is typically expected. Home-based PD treatment, either self-administered or assisted by a caregiver, may present a viable therapeutic option. These findings underscore the necessity for a large-scale randomized controlled trial (RCT) to further validate the efficacy of PBM in PD management.

Challenges and Future Directions

Despite the encouraging results, several challenges need to be addressed for the widespread adoption of PBM in PD therapy. Standardization of treatment protocols, optimization of light parameters, and identification of patient-specific factors influencing treatment response are essential. Long-term studies are warranted to assess the durability of PBM effects and its potential as a disease-modifying therapy in PD.

Conclusion

Brain photobiomodulation represents a novel and promising approach for neuroprotection in Parkinson’s disease. By targeting underlying pathological processes such as mitochondrial dysfunction, oxidative stress, and neuroinflammation, PBM has the potential to slow disease progression and improve quality of life for PD patients. Continued research efforts are needed to fully elucidate the mechanisms of PBM and optimize its therapeutic application in PD management.

References

1. Hamblin, M. R. (2016). Shining light on the head: Photobiomodulation for brain disorders. BBA Clinical, 6, 113-124.
2. Moro, C., Torres, N., El Massri, N., Ratel, D., Johnstone, D. M., Stone, J., & Benabid, A. L. (2014). Photobiomodulation preserves behaviour and midbrain dopaminergic cells from MPTP toxicity: Evidence from two mouse strains. BMC Neuroscience, 15(1), 89.
3. Salehpour, F., Mahmoudi, J., Kamari, F., Sadigh-Eteghad, S., Rasta, S. H., & Hamblin, M. R. (2018). Brain Photobiomodulation Therapy: a Narrative Review. Molecular Neurobiology, 55(8), 6601-6636.
4. Unal, O., & Tuncer, S. (2019). The effect of transcranial photobiomodulation on balance and gait in patients with Parkinson’s disease: a randomized controlled trial. Photomedicine and Laser Surgery, 37(5), 271-277.
5. Liebert A, Bicknell B, Laakso EL, Heller G, Jalilitabaei P, Tilley S, Mitrofanis J, Kiat H. Improvements in clinical signs of Parkinson’s disease using photobiomodulation: a prospective proof-of-concept study. BMC Neurol. 2021 Jul 2;21(1):256. doi: 10.1186/s12883-021-02248-y. PMID: 34215216; PMCID: PMC8249215.

Mechanisms of Brain Photobiomodulation

Mechanisms of brain photobiomodulation

PBM involves the application of low-level light, typically in the red to near-infrared spectrum, to stimulate cellular function. Light energy is absorbed by mitochondria, leading to increased adenosine triphosphate (ATP) production and upregulation of cellular metabolism. PBM also modulates oxidative stress by enhancing antioxidant defenses and reducing reactive oxygen species (ROS) production. Furthermore, PBM exerts anti-inflammatory effects by inhibiting pro-inflammatory cytokines and promoting microglial polarization towards an anti-inflammatory phenotype. These mechanisms collectively contribute to neuroprotection and neuroplasticity, making PBM a promising therapeutic approach for neurodegenerative diseases like PD.

Preclinical Evidence

Animal models of PD treated with PBM have shown improvements in motor function and preservation of dopaminergic neurons in the substantia nigra. Studies have demonstrated reduced neuroinflammation, oxidative stress, and alpha-synuclein aggregation following PBM treatment. Moreover, PBM enhances neurogenesis and synaptic plasticity, suggesting its potential to restore neuronal circuitry in PD.

Are Neurons Extra Sensitive to Light Energy?

The idea that light can influence the brain isn’t science fiction, it’s science. In recent years, the field of photobiomodulation (PBM) has uncovered how light energy, particularly in the red and near-infrared spectrum, can interact with our cells in surprisingly therapeutic ways. But are neurons, our brain’s most vital and complex cells, especially sensitive to this kind of energy?

What is Photobiomodulation?

Photobiomodulation refers to the use of specific wavelengths of light to stimulate cellular function, most notably through mitochondrial mechanisms. The most common wavelengths used are in the red (600–700 nm) and near-infrared (760–1100 nm) range. These wavelengths penetrate biological tissues and are absorbed by intracellular photoreceptors, particularly cytochrome c oxidase (CCO) in mitochondria, leading to increased ATP production, modulation of reactive oxygen species, and changes in gene expression [1].

Why Neurons Might Be More Sensitive

Neurons are highly metabolically active and rely heavily on mitochondrial function. Since they are post-mitotic and do not easily regenerate, their health is tightly linked to mitochondrial performance. This may explain why they respond especially well to light stimulation.

• High mitochondrial density: Neurons have a large number of mitochondria to support their energy needs, especially in synapses [2].
• Vulnerability to oxidative stress: The brain uses about 20% of the body’s oxygen but comprises only ~2% of its mass. PBM’s ability to regulate redox balance offers potential neuroprotection [3].
• Modulation of neuroinflammation: Light energy has been shown to reduce inflammatory markers and glial activity, both of which affect neuron health [4].

Supporting Evidence

1. Improved Cognitive Function

A randomized controlled trial found that near-infrared PBM applied to the prefrontal cortex improved attention and memory in healthy adults [5].

2. Neuroprotection After Injury

In rodent models of traumatic brain injury, PBM preserved neurons, reduced glial scarring, and stimulated regeneration [6].

3. Functional Imaging Studies

EEG and fMRI studies have shown increased brain activity and connectivity after PBM, suggesting direct effects on neural networks [7].

4. Applications in Neurodegenerative Disorders

Early human studies indicate benefits for Alzheimer’s and Parkinson’s patients, including improved mood, memory, and sleep [8].

Can Light Really Reach the Brain?

The human skull filters out much light, but near-infrared wavelengths, especially in the 810–1070 nm range, can penetrate to the cortex. Studies estimate that enough light reaches cortical tissue to stimulate a biological response, especially when higher-power or pulsed devices are used [9].

Conclusion

So, are neurons extra sensitive to light energy? Current research strongly suggests yes. Due to their high energy demands and mitochondrial density, neurons are well-positioned to benefit from photobiomodulation. Whether enhancing cognitive performance, protecting against injury, or slowing neurodegeneration, PBM appears to offer a non-invasive, promising method to support Brain wellness.

References

1. Hamblin, M.R. (2016). Shining light on the head: Photobiomodulation for brain disorders. BBA Clinical, 6, 113–124. https://doi.org/10.1016/j.bbacli.2016.09.002
2. Attwell, D., & Laughlin, S.B. (2001). An energy budget for signaling in the grey matter of the brain. Journal of Cerebral Blood Flow & Metabolism, 21(10), 1133–1145. https://doi.org/10.1097/00004647-200110000-00001
3. Sies, H. (2015). Oxidative stress: A concept in redox biology and medicine. Redox Biology, 4, 180–183. https://doi.org/10.1016/j.redox.2015.01.002
4. Salehpour, F., et al. (2018). Transcranial Photobiomodulation Therapy: A Novel Method for Neuroenhancement. Journal of Photochemistry and Photobiology B, 183, 47–55. https://doi.org/10.1016/j.jphotobiol.2018.04.007
5. Barrett, D.W., & Gonzalez-Lima, F. (2013). Transcranial infrared laser stimulation produces beneficial cognitive and emotional effects in humans. Neuroscience, 230, 13–23. https://doi.org/10.1016/j.neuroscience.2012.11.016
6. Xuan, W., et al. (2014). Transcranial low-level laser therapy improves neurological performance in traumatic brain injury in mice. PLOS ONE, 9(1), e86264. https://doi.org/10.1371/journal.pone.0086264
7. Tian, F., et al. (2016). Transcranial laser stimulation improves human cerebral oxygenation. Lasers in Surgery and Medicine, 48(4), 343–349. https://doi.org/10.1002/lsm.22470
8. Chao, L.L. (2019). Home Photobiomodulation Treatments on Cognitive and Behavioral Function in Dementia. Journal of Alzheimer’s Disease Reports, 3(1), 241–255. https://doi.org/10.3233/ADR-190135
9. https://www.vielight.com/blog/irradiance-the-key-to-effective-brain-photobiomodulation/

The nose is a gateway to important brain structures located at the underside of the brain, otherwise, unreachable from the scalp.

Can light energy reach the brain from the nose?

The layer of skull, just above the nasal cavity and below the brain (the cribriform plate) is extremely porous, delicate and thin. The thin, perforated structure of the cribriform plate can be as thin as 0.2 millimeters (other parts of the skull average 5-7mm). [1]

Due to its thin structure and multiple openings for olfactory nerves, the cribriform plate allows substantial 810nm light from an intranasal source to reach the olfactory system and nearby prefrontal cortex. [2]

In the context of brain photobiomodulation, this thin structure makes it very permeable for NIR energy to reach the ventral prefrontal medial cortex (vmPFC) a region of the brain located just above the nasal cavity. It is believed that in adult mammals, neurogenesis occurs only in the olfactory bulb and in the dentate gyrus of the hippocampus. [3]

Explainer animation with real skull anatomy and demonstration:

Why the Nose and Olfactory Bulb?

Photobiomodulation (PBM) delivered intranasally isn’t just about convenience, it’s about strategic access to the brain. The nose provides a direct channel to key brain regions via the cribriform plate, making it a highly efficient route for delivering near-infrared (NIR) light to areas that are crucial for cognition, emotion, and systemic regulation.

Let’s explore three major brain structures located near this nasal entry point:

1. Ventromedial Prefrontal Cortex (vmPFC)

Function:

• Responsible for decision-making and risk assessment

• Integrates emotional and reward-related information for complex behavioral choices

Clinical Note:
Dysfunction in the vmPFC has been associated with mood disorders, impulsivity, and impaired judgment, often seen in conditions such as depression and PTSD.

2. Olfactory Bulb

Function:

• Closely linked to memory and emotion

• Explains why certain smells can trigger vivid memories or emotional responses

Clinical Note:
The olfactory bulb is frequently one of the first regions affected in neurodegenerative diseases like Parkinson’s and Alzheimer’s, making it a valuable target for early intervention.

3. Hypothalamus

Function:

• Acts as the brain’s master regulator of homeostasis

• Controls essential functions such as temperature regulation, appetite, circadian rhythms, hormone balance, and stress response

Clinical Note:
Because of its central role in systemic regulation, the hypothalamus is an attractive therapeutic target for interventions seeking to influence brain-body balance.

Key Functions of the vmPFC

• Emotion Regulation: The vmPFC helps modulate emotional responses, often interacting with the amygdala, which is involved in processing emotions like fear and aggression. It helps downregulate excessive emotional responses.
• Decision-Making: This region is critical for value-based decision-making, where choices are made based on the predicted value of different outcomes. It weighs rewards, punishments, and social factors in decision processes.
• Social Cognition: The vmPFC contributes to understanding social norms, empathy, and moral reasoning. It helps individuals make appropriate social decisions and understand the feelings and intentions of others.
• Memory Integration: It integrates emotional and social information from past experiences to guide future behavior and decisions.

Vielight Patented Intranasal Technology

Our patented intranasal technology enables NIR light energy to diffuse through the nasal channel, to the brain’s vMPFC, which is a crucial component of the Default Mode Network.