Inventor’s Notes for Vielight “Neuro Alpha” and “Neuro Gamma”

Lew Lim, PhD, DNM, ND, MBA, FCMA, Grad.Cert.Eng.

Founder & CEO
Vielight Inc., Toronto, Canada
January 15, 2017

Introduction

The Vielight ‘Neuro Alpha’ and ‘Neuro Gamma’ are our latest brain photobiomodulation devices,
designed to enhance mental acuity and quality of life. They are low-risk near infrared (NIR)
photobiomodulation (PBM) devices that improve on the design of the Vielight ‘Neuro’.

These set of notes follow the earlier version of the Inventor’s Notes, which outline the scientific
principles behind the invention of the ‘Vielight Neuro’. The fundamental principles of PBM are shared
across all these models. I will not be repeating these principles; hence unfamiliar readers should refer to
the previous version of the Inventor’s Notes to understand these binding principles.

This paper is an exposition of the ideas and reasons behind the development of the newest models,
without any medical claims. However, steps have already been taken to test their potential to address
certain medical indications; the most advanced is that on Alzheimer’s disease (AD).

At the date of this document, the inventions are covered by several issued and pending patents. If you
are interested, you can read the ones published:

Self-administrable method, system and apparatus for non-invasive neurostimulation therapy of the
brain

Method and portable system for non-invasive, in-vivo blood irradiation light therapy

Revisiting Fundamental Design Principles of the Neuro

The main objective of my inventions is to enable anyone to enhance their general wellness and mental
acuity by trusting the body’s natural ability to heal itself through PBM.

I believe that a device should be engineered with up-to-date scientific research parameters, be easy-to-
use and portable (or ‘wearable’). The systemic and holistic effect of PBM allows for a simple intervention
with the potential to address many conditions, which are supported by many studies already.1 When we
shine near infrared (NIR) light with sufficient power density to penetrate the cranium and irradiate the
brain (transcranial), the healing possibilities cover a wide spectrum of brain disorders.2

Existing PBM devices direct photons in ways that are intuitively obvious – such as, positioning the light
energy source directly over the lesion or inflamed area. However, if we are able to direct photons into

1
the body, we can achieve a body-wide effect. The Russians have promoted injecting low energy red laser
light into the circulatory system for over 30 years.3 My idea was to simulate this process through the
nasal cavity (intranasal), which is rich in vasculature in its capillary network. There are studies to prove
its effectiveness for reducing biomarkers related to vascular risks (such as hypertension and high
cholesterol).4

More importantly for this paper, the nasal region is a gateway for photons to reach the underside of the
brain, allowing near infrared (NIR) light to reach the ventral brain areas – an unusual but logical
approach for comprehensive brain photobiomodulation.

The effectiveness of the Neuro’s intranasal diode is enhanced with its headset’s higher powered LEDs,
boosted with microchip technology. We don’t need hundreds of LEDs to trigger brain
photobiomodulation. Instead, we target fewer but higher-powered LEDs at specific nodes of a highly
interconnected brain network - the Default Mode Network (DMN). This way, we incorporate an efficient
design that is powerful, yet portable and easy to use. For more on the mechanism of action with the
parameters that I have chosen, please read the previous paper.

In summary, the main design principles are:

 Comprehensive brain photobiomodulation by

o Utilizing the intranasal pathway to the brain
o Integrating high-powered cranial LEDs
 Easy to use / portable / wearable
 Effectiveness (with no side effects)

Update on the efficacy of 810 nm

Since the publication of the original Inventor’s Notes, dated early 2015, an increasing number of PBM
studies have adopted the 810 nm wavelength to irradiate tissues of the central nervous system (CNS). A
recent investigation by Tedford et al found that the 808 nm wavelength penetrates the deepest within
CNS tissues.5 However, the 810 nm wavelength pulsed at 10 Hz has been found to produce faster wound
recovery than other parameters.6

Updates on the Neuro

We continue to reiterate that Vielight devices are low risk, suitable only for general wellness and mental
acuity with no specific medical claim. Last year FDA released its policy on low risk devices, which best
describes Vielight devices and exempts them from regulations. Health Canada has examined the devices
and allowed them to be marketed as non-medical devices (without medical claims too).

2
This is what the original Vielight Neuro looks like (Figure 1).

Figure 1: Original Vielight Neuro

The new Vielight Neuro Alpha and Gamma look like this (Figure 2)

Figure 2: Vielight Neuro Alpha and Neuro Gamma ( prototype shown, both models have the same form
factor)

The difference between the Neuro Alpha and the Neuro Gamma is in the pulse frequency. The Alpha
pulses at 10 Hz (or 10 times a second) and the Gamma at 40 Hz. The reasons for the two different
frequencies are explained in detail later.

3
The Shortcomings of the Original Vielight Neuro

While the original Neuro brought remarkable results to some users, there were some shortcomings:

 The headset does not fit certain head shapes and sizes well. Particularly, heads which are conical
or smaller than the average
 Repositioning the transcranial clusters is difficult, which we hypothesize would be helpful for
brain lesions

Additionally, I wanted to incorporate new features that were not feasible with the previous design.

New Features for Incorporation into a New Neuro (Alpha and Gamma)

Feedback from the original Neuro as well as advancement in microchip LED technology has enabled me
to implement the following modifications to the transcranial diodes:

 Boosted power density of light emitting diodes (LEDs), which would enable us to reduce the
number of LEDs required
 Improved fitting by increasing diode contact area with different-sized heads
 Allow more flexibility with the repositioning of each transcranial LED cluster

We increased the power of the rear LEDs from 41 mW/cm2 to 100 mW/cm2 to increase the photonic
penetration in brain areas covered by a thicker cranium. The use of fewer but higher-powered LEDs
enables us to increase efficiency and efficacy while keeping the device suitable for home-use.

The ‘Neuro Alpha’ and ‘Neuro Gamma’ incorporate newer and improved transcranial LED diodes. The
only difference between the two models is the pulse rate – The ‘Neuro Alpha’ pulses at 10 Hz but the
‘Neuro Gamma’ pulses at 40 Hz. The Gamma’s pulse rate is utilized for our Alzheimer’s Disease clinical
trials and the ‘Neuro Alpha’s pulse rate is ideal for general brain health, based on brainwave oscillations.

The Increase in Power Density to 100 mW/cm2

There are proponents for high powered photons delivered by lasers - up to 13W has been proposed in
using the NIR wavelength of 810 nm to treat traumatic brain injury.7 However, I believe in delivering
energy with minimal yet sufficient power to draw a positive mitochondrial response. The body has
evolved to handle power densities equivalent to the sun’s irradiation natural environment, and not
much more before risks set in. So, my aim is to deliver a power density roughly equivalent to sunlight
energy on a clear day at sea level, which averages 1050 W/m2.8 That works out to be 105mW/cm2,
rounding to 100mW/cm2. For this reason, I designed the new Neuro Alpha and Neuro Gamma to deliver
no more than 100mW/cm2. The trio of LED transcranial clusters located on the rear of the headset
utilizes a high power density, relative to the other diodes, to penetrate the thicker cranium.
Conceptually, I feel comfortable with this power level.

4
Pulsing at 40 Hz Gamma Oscillation and the Effect on Alzheimer’s disease

There is a good chance that you have a family member or know someone who has Alzheimer’s disease
(AD) – this is because it affects approximately one in three people who live past the age of 85 years.9 The
main symptom these patients exhibit manifest as impairments in working memory and declarative
memory. It is a devastating disease and I am continuing the quest to develop an intervention that could
help. The Vielight Neuro Gamma was invented for this purpose.

Many researchers believe that the answer to stopping AD lies in controlling the formation of amyloid-
beta (Aβ) load. This protein formation could be to some extent, start with the presence of sharp-wave
ripples (SWRs) in memory consolidation.10 Elevated slow Gamma (20-50 Hz) during SWRs with increased
(but not hyper) synchrony in the hippocampus (the part of the brain responsible for short term memory
management) correlates with good memory function.11 However, aberrant increases in network
excitability and compensatory inhibitory mechanisms in the hippocampus may contribute to Aβ-induced
neurological deficits in mouse models.12 Electroencephalographic (EEG) recordings in AD mouse models
indicated network hypersynchrony, primarily when gamma oscillatory activity is reduced. Therefore,
restoring gamma oscillatory may inhibit synaptic activity and reduces hypersynchrony, which reduces Aβ
formation. This would help address memory deficits, and conditions associated with AD.13

Furthermore, research has shown that neurofeedback training with Gamma oscillations can enhance the
memory and cognition in the elderly (Gamma entrainment).14 With these findings, gamma oscillation
has the potential of being both a prophylaxis against AD as well as modifying the disease. This argument
became much more convincing after the recent discovery at the Massachusetts Institute of Technology
(MIT).

Work at the MIT presented evidence that the gamma pulse frequency of 40 Hz attenuates Aβ proteins
and modulated microglia activity resulting in increased scavenging of Aβ,15 which are highly sought
conditions to modifying AD pathology. Specifically, when the mouse model was exposed to light that
flickered at 40 Hz for an hour a day for 7 days, it was found that the Aβ load in the visual cortex (VC) was
significantly reduced. The authors also found that when 40 Hz is invoked directly in the hippocampus
(memory processing area) with a chromophore, Aβ load was also significantly reduced. This suggests a
couple of reasons why the way the Neuro Gamma is set to be very promising:

1. 40 Hz flickering can reduce Aβ in the areas that has direct projection (or connection) with the
receptor area, in the case of the MIT study, the visual cortex has direct projection with the eyes.
The key memory processing area, the hippocampal area and lateral entorhinal cortex have
direct projections to the olfactory bulb (which processes smell and located above the nasal
cavity).16 17 The intranasal LED of the Neuro Gamma delivers 40 Hz flickering with considerable
energy to the olfactory bulb. Based on the expectation from the MIT study, the opportunity to
reduce the Aβ in the hippocampal areas appears excellent.
2. In the MIT study, 40 Hz flickering directly delivered to the hippocampus (albeit with an
introduced chromophore that is typical with an optogenetics study) also significantly reduces Aβ
load. We don’t know how much the Aβ load in the hippocampus would have reduced without

5
 the chromophore but it is promising. Other PBM studies with neurons in vitro had demonstrated
that delivering NIR to damaged neurons activates recovery.18 Thus, when we deliver 40 Hz NIR
to specific regions of the brain, we can reasonably expect those regions to recover. And when
we deliver 40 Hz NIR to the hubs of the Default Mode Network (DMN) which is closely
associated with AD, it should add to the efficacy of the device.19

The Importance of Portability and Ease-of-use

In my opinion, it is almost as important to develop a portable home-use device, as it is to achieve

efficacy - particularly for AD, which is strongly degenerative. The role of the genome is often not given
enough consideration in a degenerative disease like this – thus, too many researchers think (or wish)
that medication has a comparable effect, as for example, infection or injury/trauma. Infections and
traumas do not alter your genome unlike AD, which causes continuous neuronal degeneration.
Therefore, a cure would likely require consistent intervention, probably even for the rest of the patient’s
life. A possible cure could potentially involve modifying the genome sufficiently to achieve a ‘cure’ but
the side effects are not predictable and will require a long time to ascertain the long-term change. Life
would certainly be difficult if continuous doctor visits were a permanent routine. Therefore, if the
intervention is a device, it needs to be portable and easy to use at home.

I wanted to avoid dependency on the electrical mains for the sake of portability and wearability. For this
objective to be feasible, a rechargeable power battery source rationed to a few high-powered diodes as
opposed to many smaller diodes was used to maximize efficiency. For AD, we choose to do this by
directing treatment to the few key hubs of the Default Mode Network (DMN). Since AD is correlated to a
dysfunctional DMN,19 we would expect that directing an intervention to the hubs of the DMN results in
the whole DMN being treated holistically.20 Additionally, imaging work has identified AD lesions in
essentially the same positions of the DMN nodes.

Pulsing at 10 Hz Alpha Oscillation

The Alpha range (8-12 Hz) has been a favorite amongst neurofeedback practitioners to address a large
variety of factors in brain health.

Table 1 presents studies that proposed Alpha protocol training for various purposes.

6
Table 1: Summary of studies using alpha protocol training21

Even slow Alpha at 8-10 Hz is believed to be related to remembering action in semantic memory.22 The
presence of Alpha also keeps normal brain memory functions efficient by cutting out distractors.23 Alpha
power reflects maintenance of relevant memory contents rather than suppression of no-longer-relevant
memory traces.24

Therefore, Alpha entrainment appears highly versatile and its presence is associated with healthy
memory functions although Gamma is powerful to address AD specifically. I continue to assert that
Alpha, say at 10 Hz is a good all-round brain health devices.25

Alpha evoked by Gamma is positive for Alzheimer’s disease

Reduced Alpha peak power is a biomarker for AD.26 In my opinion, this correlation is not necessarily an
indication that reduced Alpha is the cause – more likely the result of AD. In our own EEG experiments,
we are discovering that successful brain entrainment with Gamma appears to elevate peak Alpha,

7
implying that the two brainwaves are correlated. It is another reason for entraining an AD brain with
Gamma oscillation.

Deciding between the Vielight Neuro Alpha and Gamma

There are many studies which discuss the possibilities of using different brain oscillation rates to treat
different conditions and trigger brain performance enhancement. To simplify the available options and
emphasize the efficacy of both of these devices, I am narrowing down the options as follows:

 Neuro Gamma (at 40 Hz) for memory deficits and AD clinical study
 Neuro Alpha (at 10 Hz) for general brain health.

Please note that none of these should be considered as devices to overcome an existing medical
condition and should not be seen as substitutes for medical care. We do not have sufficient evidence at
this point to support any medical claims – however, we are mobilizing resources and collaborating with
research institutions to run two FDA-level clinical trials and a small scale EEG validation trial this year.

Immediate Brain Response Measured with EEG and its relevance to Neurofeedback

Through client feedback and research, we discovered that the brain responds to PBM stimulation via
Vielight NIR technology. However, I was unsure if we could observe the process in real-time. Initially, I
observed this phenomenon while using the original Neuro with the Brainmaster Avatar neurofeedback
system running during the 2015 International Society for Neurofeedback & Research (ISNR) Conference
– though, I was unsure if it was a placebo effect.

I was introduced to the idea behind integrating photobiomodulation with neurofeedback by Marvin
Berman, from the Quietmind Foundation. He conducted his own neurofeedback tests with the Vielight
810 intranasal device, as well as the Neuro, initially. He used the Neuroguide software which presented
clear improvements in QEEG brainmap profiles (some of these were presented in the earlier Inventor’s
Notes). Back then, we did not have the opportunity to conduct controlled studies and measure
statistical significance. That is something we are starting to do but prior, we took a risk and decided to
present our first public live demo at the 2016 ISNR Conference. Here is a link to the demo -
https://www.youtube.com/watch?v=Aefz0tNtfpI&feature=youtu.be.

If you are a neurofeedback practitioner, you should really watch Robert Thatcher’s (Developer of the
Neuroguide technology) EEG discoveries with the Vielight Neuro recorded live on video:

https://www.youtube.com/watch?v=x3aEWWGxMJU
https://www.youtube.com/watch?v=jvRK7_1kmks

8
These experiments partly answer the question on whether the brain responds to NIR from the Neuro,
and whether the response is immediate. We will be conducting a small scale, clinical grade, double-blind
study to validate this effect. Eventually with more EEG experiments, we will also know how well it
performs against other non-invasive neurostimulation modalities such as the Transcranial Direct Current
Stimulation (tDCS) and Transcranial Magnetic Stimulation (TMS). In the meantime, our neuroscience lab
at Vielight continues to experiment with integrating PBM and EEG on Vielight systems. It explores new
possibilities in regards to what we can do with our technology in the service of enhancing the quality of
life for many where there is no effective medical intervention.

Our Current Research with EEG

Based on early anecdotal feedback, the difference between the Neuro Alpha and Neuro Gamma appears
to be that that Neuro Alpha has a more calming effect than the Neuro Gamma. More data is, of course,
required to be sure of this particular difference. However, as suggested in the literature, alpha brain
entrainment reduces anxiety and has healing properties. Although gamma entrainment presently
suggests more restlessness, the data collected at this point in time has shown elevated alpha brain
oscillations when the brain was subjected to gamma oscillations at 40 Hz.

For a person with cognitive impairment, this is what we want. Brains of people with mild cognitive
impairment (MCI – possibly in the early symptoms of AD) have relatively lower alpha power.27 If 40 Hz
entrainment restores this alpha power deficit, then we hypothesize that positive brain modulation to
overcome cognitive impairment is taking place. It is therefore relevant to AD by contributing to the
reduction of the Aβ load and activating microglia activity as presented by the MIT study.

In any event, it is significant to have evidence that the brain responds in real-time to NIR stimulation
from Vielight technology because:

1. It overcomes uncertainty if Vielight NIR stimulation has an observable effect on the brain.
2. Real time response to our technology can be demonstrated in real time.
3. We now have a convenient tool to better understand the effect of NIR from a Vielight device.
This enables us to fine-tune parameters for more effective treatments.

Neurofeedback and Intranasal-Transcranial Photobiomodulation

Evidence is growing that this modality could be a tool to reduce the treatment target time of
neurofeedback (NFB) practitioners. One of the challenges of NFB, for patients and practitioners alike, is
the time involved and the benefits are often not long-lasting. It may take several months to see the
desired improvements.28 On the other hand, NIR PBM with Vielight devices often produces quick
observable outcomes, both on modern software such as the Neuroguide and the Brainmaster, or in
psychological or psychiatric assessments. We have produced significantly improved cognitive

9
assessments for AD in a matter of weeks in clinical settings in our pilot study, done in collaboration with
Boston University School of Medicine and Harvard Medical School (Link).

Margaret Naeser’s lab at the Boston University School of Medicine have also started to show positive
outcomes for traumatic brain injury with our Vielight 810 intranasal device.29 Other studies have shown
that shining NIR to the brain also improves insults from strokes, Parkinson’s disease and depression.2

Evidence for PBM on Alzheimer’s disease

I have discussed the viability of the various parameters earlier, and in particular entrainment at 40 Hz to
address AD. We are now investing in clinical trials to validate this endpoint. However, this is quite the
task for a fledgling company like Vielight, considering that 99.5 percent of AD drug trials have failed after
investments of hundreds of millions of dollars. Is it rational or is it foolhardy bravado? I would consider it
a calculated risk.

Evidence that PBM could help with AD actually goes back to a study published in 2011, when it was
found that when a 808 nm low level laser beam was directed to the brain of mice, the Aβ biomarker
count was reduced and behavior deficit was also improved.30 Another study used a longer wavelength of
1072 nm and produced a similar outcome.31 Yet another mouse-model study published in 2014
confirmed the results of these two studies.32 If we seek to do something about AD that can be
represented by a reduction of the Aβ biomarkers, these studies have laid the path. Potentially, PBM not
only improves the symptoms through improved cognition; top researchers continue to believe that
reducing the Aβ plaques is still the gold standard to modifying the disease.33 However, as every
researcher can tell you, and especially so in the world of AD research animal study results are no
indication that they will be repeated in human.

In 2011, I started my own investigation in regards to the potential of PBM on dementia and AD with the
Vielight 810 Infrared (intranasal-only) device. The results were very encouraging but they were largely
anecdotal. We decided to step up our game with clinical evidence.

Eventually with the aid of Anita Saltmarche (principal investigator), Kai Fai Ho (clinical statistician),
Margaret Naeser (Research Professor of Neurology at Boston University School of Medicine) and
Michael Hamblin (Associate Professor at Harvard Medical School), we managed to complete a case
series study showing significant improvement in 5 people with cognitive impairment associated with AD.
At the time of writing, the paper has been accepted for publication. The protocol involved a
combination of using the Neuro and the ‘Vielight 810 Infrared’ intranasal-only device over a 12-week
period.

The quality of evidence has improved but I recognize that the sample is too small, and the study period
too short. At the time of writing, plans are underway to do two clinical grade FDA approved studies – a
pilot study involving 40 patients and a longer-term study involving 226 patients. They will be
randomized, double-blind placebo-controlled studies. The subject device will be the Neuro Gamma.

10
Evidence on traumatic brain injury and other insults

Research on the effect of PBM on human brain insults for traumatic brain injury (TBI) and strokes have a
longer history than for dementia and AD. There are studies on other neuro-pathologies but they were
mainly performed on animals - human-based studies, such as depression, are recent. Recently Michael
Hamblin provided an excellent overview of the research that has been done with transcranial PBM.34

To many, it is hard to believe that anyone can claim that a single, simple intervention can address so
many brain insults. When light energy with the appropriate parameters is delivered to the brain, it
modulates systemic effects to restore normal brain functions. Vielight has received anecdotal reports of
improvements in various brain functions but I have to reiterate that we need to have evidence from
controlled studies before we can substantiate medical claims. In any event, the seemingly expected
outcomes stem from the fundamental premise that as long as the mitochondria of a sub-functioning
neuron receives red or NIR photons of certain parameters35, we can activate the healing process. AD is
just another one of these pathologies - with a strong neurodegenerative element. Based on the history
of evidence, I would have been surprised if we don’t get any positive outcome for AD.

The Feasibility of Photobiomodulation vis-à-vis Pharmacotherapy focusing on Alzheimer’s disease

Let’s see how well the mechanisms of Vielight PBM holds up against the pharmacological (drug)
approach.

A drug intervention needs a clear protein target so that it can attack it. Unfortunately, AD involves
multiple proteins. Researchers have categorize them into two major pathways, one that take the path of
the amyloid beta cascade, and the other, the tau protein misfolding that leads to neurofibrillary (NFB)
tangles. This is well presented in the Figure 3 below.

11
Figure 3: Multiple Pathogenesis of Alzheimer’s Disease36

Source: Frigerio et al (2016). Alzheimer’s Disease Mechanisms and Emerging Roads to Novel
Therapeutics. Annu. Rev. Neurosci. 39.

The effect of PBM is fundamentally different from a drug intervention. I have mentioned that it is
systemic, as supported by many studies34. It appears unconfined to specific conditions and appears to
reestablish functional homeostasis throughout the body (and the brain).37 Based on this hypothesis, one
single intervention with PBM is equivalent to using multiple pharmacological interventions. Because it
activates the body’s innate ability to heal, as opposed to directly and synthetically modifying target
molecules, there is also no major side effect. For AD, where there pathogenesis is highly complex, the
effective intervention could be one which activates systemic homeostatic restoration. PBM fits the bill.

Research in modifying AD is trending towards an intervention that effectively modifies the disease in
early stage – before the onset of symptoms (asymptomatic), and before influentual factors such as the
APoE 4 gene, other genetic factors, age, circulating factors, etc take hold of the pathology and catalyzes
the genesis of Aβ deposits and neurofibrillary tangles. Figure 4a presents the current thinking of
researchers as to the point of an intervention from a “dynamic process of progression”.38

12
Figure 4a: AD Risk Model for Drug Development Target

Source: Dubois et al (2016). Preclinical Alzheimer’s disease: Definition, natural history, and diagnostic
criteria. Alz & Dem; 12: 292-323.

On the other hand, PBM can give the opportunity to intervene at any point of the pathology – both at
the asymptomatic stage (as a prophylaxis) as well as after the presentation of symptoms (when no drug
has ever shown to be effective). See Figure 4b.

13
Figure 4b: PBM is Agnostic to AD Risk Stage

Source: Dubois et al (2016). Preclinical Alzheimer’s disease: Definition, natural history, and diagnostic
criteria. Alz & Dem; 12: 292-323 (Modified)

Future Directions

The parameters utilized in the present Vielight devices have been determined based on my
understanding of PBM and neuroscience. Although results have generally been very good, they can be
improved if we incorporate more options within the parameters. We have a plan in place to incorporate
more adjustable diode placements, adjustable power, and adjustable pulse frequencies. These will be
controllable with a tablet or a smart phone.

We also plan to explore other neurological conditions, such as traumatic brain injury, stroke and
Parkinson’s disease.

Conclusion

There is a lot of promise in the application of PBM for a variety of neurological and psychiatric
conditions, all fundamentally based on the foundation of mitochondrial response to red and NIR light
stimulation with the appropriate power density and pulse rate. These opportunities have been refined
with adjustments to the pulse frequency, allowing the brain to be entrained with the options of
different pulse frequencies. The use of EEG technology with the Vielight devices allows us to better

14
understand and propose various fine-tuned set f parameters to optimize the treatment for specific
conditions.

For now, I am focusing on refining and increasing research on the effects of the Vielight Neuro Gamma
on AD. Later, we plan on investigation the efficacy of PBM against neurological conditions such as
Parkinson’s disease, stroke, traumatic brain injury, sleep and addiction. We can’t be certain of the
benefits to users until we expand the clinical trial to cover new conditions, which will always be a
challenging proposition for a small company like Vielight. But we are aiming high and plan to do more of
these as we grow. The future is bright.

In summary:

• Neuro Gamma (40 Hz) for memory deficits and AD clinical study
• Neuro Alpha (10 Hz) for general brain health.

Acknowledgment

We received lots of helpful feedback from researchers, customers and a constant flow of ideas from the
dedicated Vielight team, which we continuously incorporate to improve our technology.

References

1
Chung H, Dai T, Sharma SK, Huang YY, Carroll JD, Hamblin MR (2012). The nuts and bolts of low-level laser (light)
therapy. Ann Biomed Eng. 40(2):516-33.
2
Hamblin MR (2016). Shining light on the head: Photobiomodulation for brain disorders. BBA Clin. 6:113-124.
3
Moshkovska T, Mayberry J (2005). It is time to test low level laser therapy in Great Britain. Postgrad Med J.
81(957): 436–441.
4
Liu TCY, Cheng L, Su WJ, et al (2012). Randomized, Double-Blind, and Placebo-Controlled Clinic Report of
Intranasal Low-Intensity Laser Therapy on Vascular Diseases. Int Jnl Photoenergy. Article ID 489713.
5
Tedford CE, DeLapp S, Jacques S, Anders J. (2015). Quantitative analysis of transcranial and intraparenchymal
light penetration in human cadaver brain tissue. Lasers Surg Med. 2015 Apr;47(4):312-22.
6
Keshri GK, Gupta A, Yadav A, et al (2016). Photobiomodulation with Pulsed and Continuous Wave Near-Infrared
Laser (810 nm, Al-Ga-As) Augments Dermal Wound Healing in Immunosuppressed Rats. PLoS One. 11(11)
7
Henderson TA (2016). Multi-watt near-infrared light therapy as a neuroregenerative treatment for traumatic
brain injury. Neural Regen Res. 11:563-5.

15
8
Introduction to Solar Radiation. Newport Corporation ( 2016). Retrieved from
https://www.newport.com/t/introduction-to-solar-radiation.
9
Alzheimer’s Association (2016). Retrieved from: http://www.alz.org/alzheimers_disease_causes_risk_factors.asp
10
Girardeau G, Zugaro M (2011). Hippocampal ripples and memory consolidation. Curr Opin Neurobiol. 21(3):452-
9.
11
Carr MF, Jadhav SP, Frank LM (2011). Hippocampal replay in the awake state: a potential substrate for memory
consolidation and retrieval. Nat Neurosci. 14(2):147-53.

12
Palop JJ, Chin J, Roberson ED, Wang J, Thwi, MT, et al. (2007). Aberrant Excitatory Neuronal Activity and
Compensatory Remodeling of Inhibitory Hippocampal Circuits in Mouse Models of Alzheimer's Disease. Neuron.
55:697-711

13
Verret L, Mann E, Hang G, Barth A, Cobos I, et al. (2012). Inhibitory Interneuron Deficit Links Altered Network
Activity and Cognitive Dysfunction in Alzheimer Model. Cell. 149:708-21
14
Staufenbiel SM, Brouwer AM, Keizer AW, van Wouwe NC (2014). Effect of beta and gamma neurofeedback on
memory and intelligence in the elderly. Biol Psychol. 95:74-85.
15
Iaccarino HF, Singer AC, Martorell AJ, et al (2016). Gamma frequency entrainment attenuates amyloid load and
modifies microglia. Nature 540(7632): 230-235.
16
Scott JW, McBride RL, Schneider SP (1980). The organization of projections from the olfactory bulb to the
piriform cortex and olfactory tubercle in the rat. J Comp Neurol. 194(3):519-34.
17
Khan UA, Liu L, Provenzano FA, Berman DE, et al (2014). Molecular drivers and cortical spread of lateral
entorhinal cortex dysfunction in preclinical Alzheimer's disease. Nature Neuroscience. 17: 304–311.
18
Giuliani A, Lorenzini L, Gallamini M, et al (2009). Low infrared laser light irradiation on cultured neural cells:
effects on mitochondria and cell viability after oxidative stress. BMC Com Alt Med. 9:8.
19
Buckner, R. L.; Andrews-Hanna, J. R.; Schacter, D. L. (2008). The Brain's Default Network: Anatomy, Function, and
Relevance to Disease. Annals of the New York Academy of Sciences. 1124 (1): 1–38.
20
Andrews-Hanna, Jessica R.; Smallwood J, et al (2014). The default network and self-generated thought:
component processes, dynamic control, and clinical relevance. Annals of the New York Academy of Sciences. 1316
(1): 29–52.
21
Marzbani H, Marateb HR, Mansourian M (2016). Neurofeedback: A Comprehensive Review on System Design,
Methodology and Clinical Applications. Basic Clin Neurosci. 7(2):143-58.
22
Dempster, T. (2012). An investigation into the optimum training paradigm for alpha electroencephalographic
biofeedback (PhD Thesis). U.K.: Canterbury Christ Church University.
23
Bonnefond M, Jensen O (2012). Alpha oscillations serve to protect working memory maintenance against
anticipated distracters. Curr Biol. 22(20):1969-74.
24
Manza P, Hau CLV, Leung HC (2014). Alpha Power Gates Relevant Information during Working Memory
Updating. J Neurosc. 34 (17) 5998-6002.

16
25
Ando T, Xuan W, Xu T, Dai T, et al (2011). Comparison of Therapeutic Effects between Pulsed and Continuous
Wave 810 nm Wavelength Laser Irradiation for Traumatic Brain Injury in Mice. Plos One. 6(10).
26
Kwak YT (2006). Quantitative EEG findings in different stages of Alzheimer's disease. J Clin Neurophysiol.
23(5):456-61.
27
López-Sanz D, Bruña R, Garcés P, et al (2016). Alpha band disruption in the AD-continuum starts in the Subjective
Cognitive Decline stage: a MEG study. Scientific Reports 6, Article number: 37685.
28
Mauro, T., & Cermak, S. A. (2006). The Everything Parent’s Guide to Sensory Integration Disorder: Get the Right
Diagnosis, Understand Treatments, and Advocate for Your Child. USA: Adams Media Corporation.
29
Naeser MA, Martin PI, Ho MD, et al (2016). Transcranial, Red/Near-Infrared Light-Emitting Diode Therapy to
Improve Cognition in Chronic Traumatic Brain Injury. Photomed Laser Surg. 34(12):610-626.
30
De Taboada L, Yu J, El-Amouri S, et al (2011). Transcranial laser therapy attenuates amyloid-beta peptide
neuropathology in amyloid-beta protein precursor transgenic mice. J Alzheimers Dis. 23(3):521-35.
31
Grillo SL, Duggett NA, Ennaceur A, Chazot PL (2013). Non-invasive infra-red therapy (1072 nm) reduces beta-
amyloid protein levels in the brain of an Alzheimer’s disease mouse model, TASTPM. J Photochem Photobiol B
2013, 123:13–22.
32
Purushothuman S, Johnstone DM, Nandasena C, Mitrofinas J and Stone J (2014). Photobiomodulation with near
infrared light mitigates Alzheimer’s disease-related pathology in cerebral cortex – evidence from two transgenic
mouse models. Alzheimer’s Research & Therapy. 6:2.
33
Reiman EM (2017). Alzheimer disease in 2016: Putting AD treatments and biomarkers to the test. Nat Rev
Rheumatol. Jan 13.
34
Hamblin MR (2016). Shining light on the head: Photobiomodulation for brain disorders. BBA Clin. 6:113-124.
35
De Freitas, Hamblin MR (2016). Proposed Mechanism of Photobiomodulation or Low Level Light Therapy. IEEE
Journal of Selected Topics. 22:3.
36
Frigerio et al (2016). Alzheimer’s Disease Mechanisms and Emerging Roads to Novel Therapeutics. Annu. Rev.
Neurosci. 39.
37
Liu TCY, Wu DF, Zhu L, Peng P, et al (2014). Microenvironment Dependent Photobiomodulation on Function-
Specific Signal Transduction Pathways. International Journal of Photoenergy; 1-8.
38
Dubois B, Hampel H, Feldman HH, et al (2016). Preclinical Alzheimer’s disease: Definition, natural history, and
diagnostic criteria. Alz & Dem; 12: 292-323.

17