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24 people improve by 70% with 7 days of Flickering Light & Sound
Posted: Friday, February 7, 2020 1:26 PM
Joined: 2/17/2019
Posts: 380



A non-invasive therapy that just might outperform drugs


All subjects exhibited improvement of cognitive function as expressed by testing with an average improvement of 73.6% across all exams. 

92% of subjects were described as “improved” by their family and or caregivers, inclusive of “mood, disposition, and engagement” as defined in administration of a post therapy interview.


Subjects average MoCA results improved from 15 out of 30, to 25.5 out of 30, for a 70% change.

Subjects average Mini-Cog™ results improved from 2 out of 5, to 4 out of 5, for a 100% change.

Subjects average SSLH results improved from 8 out of 15, to 12 out of 15, for a 50.9% change.

Notable observations were that the memory impairment component of the subjects was the most dramatically improved, followed by executive functioning.



Effects of Specific Flashing Light Therapy for the Treatment of Cognitive Impairment Associated with Alzheimer’s Disease

B. Beshaw 2018


Would you try an experimental treatment that preliminary tests indicate helps to improve memory and cognitive function in most cases?

 If this treatment is based in rigorous scientific investigation, is not a drug, is totally safe, non-invasive, and has no side effects; would that effect your decision? 

Flashing light therapy just might be that treatment.  

Lane Simonian
Posted: Friday, February 7, 2020 2:07 PM
Joined: 12/12/2011
Posts: 5137

It looks to me like they have figured out the right frequency and delivery systems.
Lane Simonian
Posted: Friday, February 7, 2020 3:10 PM
Joined: 12/12/2011
Posts: 5137

One part of photobiomodulation is removing amyloid.  But this is probably the more important aspect:

Excitotoxicity contributes to brain damage after stroke, traumatic brain injury, and neurodegenerative diseases, and is also involved in spinal cord injury. We tested whether low level laser (light) therapy (LLLT) at 810 nm could protect primary murine cultured cortical neurons against excitotoxicity in vitro produced by addition of glutamate, NMDA or kainate. Although the prevention of cell death was modest but significant, LLLT (3 J/cm(2) delivered at 25 mW/cm(2) over 2 min) gave highly significant benefits in increasing ATP, raising mitochondrial membrane potential, reducing intracellular calcium concentrations, reducing oxidative stress and reducing nitric oxide. The action of LLLT in abrogating excitotoxicity may play a role in explaining its beneficial effects in diverse central nervous system pathologies.

The same is also likely true for flickering lights.  

Mice performed better on the Barnes maze and the What-Where-Which task, and hippocampal levels of antioxidant enzymes were increased and oxidative stress biomarkers were decreased. In studies of the effect of PBM on traumatized muscle, PBM has been shown to be effective in regulating the amount of cytokine-inducible nitric oxide synthase (iNOS) produced by the cell. This is important because excessive amounts of iNOS can lead to the excessive production of NO, which would then signal increased production of the ROS/RNS called peroxynitrite, leading to an increase in oxidative stress. Specifically, PBM could reduce peroxynitrite [], while still preserving the positive effects of other isoforms of NO synthase, such as endothelial nitric oxygen synthase (eNOS), which is the species primarily responsible for the vasodilating effects of PBM [].

So light reduces the damaging forms of nitric oxide (inducible nitric oxide which combines with superoxide anions to produce peroxynitrite; which in turns leads to DNA damage, loss of neurotransmitters, inflammation, and the death of neurons, synapses, and axons) while preserving endothelial nitric oxide which leads to improved blood flow in the brain and the regeneration of neurons, synapses, and axons in the hippocampus.

Lane Simonian
Posted: Saturday, February 8, 2020 9:55 AM
Joined: 12/12/2011
Posts: 5137

A bit more: flickering lights activate cyclic AMP which produces the following results:

Cyclic AMP promotes neuronal survival by phosphorylation of glycogen synthase kinase 3beta.

Agents that elevate intracellular cyclic AMP (cAMP) levels promote neuronal survival in a manner independent of neurotrophic factors. Inhibitors of phosphatidylinositol 3 kinase and dominant-inactive mutants of the protein kinase Akt do not block the survival effects of cAMP, suggesting that another signaling pathway is involved [this is good because the inhibition of the phosphatidyinositol 3 kinase/Akt pathway is one of the main problems in Alzheiemer's disease]...These data suggest that activated PKA directly phosphorylates GSK-3beta and inhibits its apoptotic activity in neurons.

Here are some of the results when you inhibit GSK3:

Inhibit tau phosphorylation

Inhibit Amyloid-beta formation

Increase Amyloid-beta clearance

Increase Hippocampal neurogenesis

I think that we have another winner in the treatment of Alzheimer's disease.