BDNF, Neuroplasticity & Near-Infrared Light

Brain-derived neurotrophic factor, commonly known as BDNF, is one of the most widely studied proteins in neuroscience. It participates in the way neurons develop, communicate and adapt to activity.

Researchers studying photobiomodulation (PBM) have examined whether certain red and near-infrared light exposures may influence cellular pathways associated with BDNF. This is an evolving research area involving laboratory models, animal studies and a smaller body of human evidence.

Understanding the subject requires an important distinction: BDNF is not a “repair fluid,” and light has not been shown to switch on an automatic brain-rebuilding process.

What Is BDNF?

BDNF belongs to a family of signaling proteins called neurotrophins. It is produced in several parts of the nervous system and is especially relevant to neurons and synapses—the communication points between nerve cells.

BDNF participates in processes including:

Neuronal development and maintenance
Activity-dependent synaptic signaling
Regulation of synaptic strength
Formation and stabilization of certain neural connections
Long-term potentiation, or LTP

LTP is a sustained change in synaptic efficiency frequently studied as a cellular model related to learning and memory. This does not mean that raising a single biomarker automatically improves memory or other aspects of cognition. Neuroplasticity depends on coordinated activity across many genes, proteins, cell types and neural networks.[1,2]

BDNF Is More Complex Than “More Is Better”

BDNF is first produced as a precursor called proBDNF. It can then be processed into mature BDNF.

These forms do not necessarily produce identical effects:

Mature BDNF commonly binds to the TrkB receptor and participates in pathways associated with synaptic activity and plasticity.
ProBDNF can interact with other receptors, including p75NTR, and may have different or sometimes opposing effects.

The biological result depends on where BDNF is produced, how it is processed, when it is released, which receptors are present and what the surrounding neurons are doing.

For this reason, describing BDNF as a general “growth factor” or “brain repair factor” is incomplete. A measured increase in BDNF expression does not, by itself, demonstrate the formation of useful neural connections or a meaningful change in human performance.

How BDNF–TrkB Signaling Works

When mature BDNF binds to a compatible TrkB receptor, it can activate several intracellular signaling pathways. Frequently studied examples include:

PI3K–Akt signaling
Ras–MAPK/ERK signaling
PLCγ signaling

These pathways participate in protein synthesis, calcium signaling, gene regulation and synaptic activity. BDNF–TrkB signaling also interacts with CREB, a transcription factor involved in regulating activity-dependent genes.

BDNF release is not distributed uniformly throughout the brain. Its production and secretion can be influenced by neuronal activity, and its effects may be concentrated around active synapses.[2,3]

This activity dependence is an important part of normal neuroplasticity. It should not be interpreted as evidence that an external light source can precisely direct BDNF to a chosen location or reconstruct a specific neural circuit.

Why Photobiomodulation Researchers Study BDNF

PBM research examines how defined red or near-infrared light exposures interact with cellular photoacceptors and signaling systems.

Proposed upstream mechanisms include changes involving:

Mitochondrial activity
ATP-related processes
Redox signaling
Nitric oxide
Calcium signaling
Transcription factors such as CREB

Because CREB and related signaling pathways can participate in regulating BDNF expression, researchers have investigated BDNF as one possible downstream marker of PBM exposure.[4]

The proposed relationship can be summarized cautiously as:

Light exposure → cellular and mitochondrial signaling → possible changes in gene regulation → possible changes in BDNF-related activity

Each arrow represents an area of continuing research. The sequence is not a guaranteed response, and it should not be treated as a complete explanation of how near-infrared light interacts with the brain.

What Has Research Observed?

Different levels of evidence need to be considered separately.

Laboratory and tissue studies

A 2019 study examined 660nm LED exposure in a hippocampal cell line and mouse hippocampal tissue cultures. Under that study’s specific conditions, researchers reported changes in ERK and CREB signaling alongside increased BDNF expression.[5]

This was a laboratory and ex vivo tissue study—not a clinical study in the living human brain. It also used 660nm light and a defined experimental protocol. Its results cannot automatically be transferred to 810nm light, another exposure level or a consumer device.

Preclinical animal research

Some animal studies have reported changes in BDNF expression and markers related to synaptic activity following specific PBM protocols. These studies help researchers develop hypotheses and identify pathways worth investigating.

Animal findings remain preclinical evidence. Differences in anatomy, tissue thickness, light delivery, dose and biology limit direct comparison with humans.

Human research

Human evidence connecting transcranial PBM and BDNF remains limited.

A 2024 randomized study in adults over 50 reported changes in serum BDNF following a specific multi-session red and near-infrared light protocol.[6] However, serum BDNF is a peripheral biomarker. It does not directly measure the amount, location or activity of BDNF inside the brain.

The study also evaluated a particular population, device configuration and treatment schedule. Its findings require further replication and cannot be generalized to every wavelength, protocol or product.

Why Wavelength and Parameters Matter

PBM studies use a wide range of light-delivery parameters:

Wavelength
Irradiance
Radiant exposure
Session duration
Illuminated area
Continuous or pulsed delivery
Pulse frequency and duty cycle
Number and timing of sessions
Position of the light source
Characteristics of the target tissue

These factors work together. A biological observation made with 660nm light cannot be assumed to occur with 810nm, and a result from one exposure schedule cannot be applied to another without supporting evidence.

Research has also not established that 40Hz light universally increases BDNF or directs its release to active synapses in the human brain. Pulse frequency is one experimental variable among many, not proof of a particular cellular outcome.

What This Means for Brainlume

Brainlume uses 810nm near-infrared light delivered through six head-worn light modules. It includes 10Hz and 40Hz operating modes with a standard 20-minute session.

These specifications describe how the device delivers light. They do not demonstrate that Brainlume increases BDNF, activates TrkB signaling or changes synaptic structure in an individual user.

Research conducted with different wavelengths, devices, populations or laboratory models should not be presented as direct evidence of Brainlume’s effects.

Brainlume’s design is informed by the wider PBM research landscape while remaining focused on simple, repeatable daily brain-wellness routines.

A More Accurate Scientific Perspective

BDNF is an important part of the biology of synaptic plasticity, but it does not operate alone. Its effects depend on molecular form, receptor activity, timing, location and the wider state of the neural network.

Current research supports several careful conclusions:

BDNF participates in activity-dependent synaptic signaling and plasticity.
BDNF–TrkB signaling interacts with pathways including ERK, Akt, PLCγ and CREB.
Some laboratory and preclinical PBM studies have reported changes in BDNF-related markers.
Human evidence remains limited and protocol-specific.
A change in peripheral BDNF does not directly measure BDNF activity inside the brain.
Findings from one wavelength or research device cannot automatically be applied to another product.

The responsible interpretation is not that light rebuilds or repairs the brain. It is that researchers are continuing to study whether particular light exposures interact with cellular pathways that also participate in neuroplasticity.

References

Leal G, Bramham CR, Duarte CB. “BDNF and Hippocampal Synaptic Plasticity.” Vitamins and Hormones. 2017;104:153–195. https://doi.org/10.1016/bs.vh.2016.10.004
Waterhouse EG, Xu B. “New Insights into the Role of Brain-Derived Neurotrophic Factor in Synaptic Plasticity.” Molecular and Cellular Neuroscience. 2009;42(2):81–89. https://doi.org/10.1016/j.mcn.2009.06.009
Minichiello L. “TrkB Signalling Pathways in LTP and Learning.” Nature Reviews Neuroscience. 2009;10:850–860. https://doi.org/10.1038/nrn2738
de Freitas LF, Hamblin MR. “Proposed Mechanisms of Photobiomodulation or Low-Level Light Therapy.” IEEE Journal of Selected Topics in Quantum Electronics. 2016;22(3):7000417. https://doi.org/10.1109/JSTQE.2016.2561201
Heo JC, Park JA, Kim DK, Lee JH. “Photobiomodulation (660nm) Therapy Reduces Oxidative Stress and Induces BDNF Expression in the Hippocampus.” Scientific Reports. 2019;9:10114. https://doi.org/10.1038/s41598-019-46490-4
de Oliveira BH, et al. “Transcranial Photobiomodulation Increases Cognition and Serum BDNF Levels in Adults Over 50 Years: A Randomized, Double-Blind, Placebo-Controlled Trial.” Journal of Photochemistry and Photobiology B: Biology. 2024;260:113041. https://doi.org/10.1016/j.jphotobiol.2024.113041

Disclaimer: This article is provided for general educational purposes. The research discussed includes laboratory, preclinical and human studies conducted with different wavelengths, devices and parameters. It should not be interpreted as evidence that Brainlume produces the same biological responses. Brainlume is a general wellness device and is not intended to diagnose, treat, cure or prevent any disease or medical condition.