Video used with permission from the Picower Institute for Learning and Memory at MIT
How the VLED Device Works
VLED + Lamp + User = Positive Results
The VLED device may stop or reduce the progression of Alzheimer’s, Parkinson’s and Dementia related diseases. This occurs by maintaining a specific light frequency and amplitude to optimally activate the Microglial Cells in the brain.
The photons of light, having a specific energy level, are transported via the retina, to the occipital lobe of the brain. This energy is then discharged as flashes across the brain’s surface at the desired Gamma Wave energy level.
The photons of light, having a specific energy level, enter the eye and are converted to electrons in the eye. These electrons, having the same energy as the photon, are transported via electrochemical reactions through the retina, down the optic nerve, to the occipital lobe of the brain. This energy is then discharged as electro chemical “flashes” across the brain surface at the desired Gamma Wave energy level.
This Gamma wave energy level is required to activate the Microglial Cells. The Microglial Cells are essential for the removal of Amyloid beta protein, the primary cause of Alzheimer’s, Parkinson’s, ALS, PSP and Dementia related amyloidosis disease.
What are Microglia Cells?
Microglia are a type of neuroglia (glial) cell located throughout the brain and spinal cord. Microglia account for 10–15% of all cells found within the brain. An adult brain contains about 100 billion nerve cells, or neurons, with branches that connect at more than 100 trillion points. Scientists call this dense, branching network a “neuron forest.”
Microglia are the resident “debris cleaning” cells. They act as the first and main form of active immune defense in the central nervous system (CNS). Microglia (and other neuroglia including astrocytes) are distributed in large non-overlapping regions throughout the CNS. Microglia are constantly scavenging the CNS for cellular debris, pathogens and Aβ plaques, damaged or unnecessary neurons and synapses, and infectious agents. Microglia must be efficient and healthy to prevent potentially fatal damage. Microglia are extremely sensitive to even slight changes in diet, medications, energy levels and pathological changes in the CNS.
What is Amyloid Beta Protein?
Amyloid beta (Aβ or Abeta) proteins, (peptides of 36–43 amino acids), and amyloid plaques are involved in the progression of Alzheimer’s disease. Aβ molecules can aggregate to form flexible soluble oligomers, like polymers or plastic, which may exist in several forms. It is now believed that certain misfolded oligomers (known as “seeds”) can induce other Aβ molecules to also take the misfolded oligomeric form, leading to a chain reaction akin to a prion (“mad cow”) infection. The seeds or the resulting amyloid plaques are toxic to nerve cells. These plaques will accumulate on the neuron cell membrane and along the axion, slowly killing the neuron cell. The other protein implicated in Alzheimer’s disease, tau protein, also forms such prion-like misfolded oligomers, and there is some evidence that misfolded Aβ can induce tau to misfold.
Tweaking Electrical Activity in the Brain Impairs and Restores Mouse Social Behaviors
Researchers pioneer technique to test how changes in brain activity may produce autism symptoms. Researchers altered the social behavior of mice by using light to manipulate electrical activity in a brain region involved in learning and socializing. The study, published this fall in Nature, bolsters the theory that autism may stem from an imbalance in the natural signals that excite or dampen activity within the brain. The study also offers a new approach to creating animal models of autism—crucial for testing promising medicines that might relieve disabling symptoms.
Using a technique, he pioneered and dubbed “optogenetics,” Stanford University psychiatrist Karl Deisseroth, M.D., Ph.D., and his colleagues engineered mice to produce light-sensitive proteins in the prefrontal cortex—a region involved in learning and social behavior. In a typical brain, some cells send signals that excite brain activity while other cells send signals that quiet it. In the optogenetic mice, excitatory brain cells respond to blue light and inhibitory brain cells respond to yellow light.
As a result, the researchers could dial up or dial down the level of activity in a mouse’s prefrontal cortex with pulses of light sent through a fiber optic cable implanted in its brain. The light’s effect lasted up to a half hour, enabling the researchers to remove the visible portion of the fiber optic implant and observe how the mice interacted with new mice or objects placed in their enclosures.
When the mice were exposed to blue light alone, they abruptly lost interest in socializing with new mice. By contrast, typical mice readily approach and sniff newcomers. However, the blue-light stimulated mice did not display other deficits such as difficulty adjusting to new objects placed in their cages.
When both excitatory and inhibitory cells were turned on simultaneously (by exposure to blue and yellow light), the mice resumed typical social behaviors.
The findings support a theory that autism stems from a dysregulation of normal brain signaling. Other evidence supporting this idea includes the fact that about one-third of those with autism also suffer seizures, a result of excessive electrical activity in the brain. In addition, several of the altered genes associated with autism play a role in brain signaling. Also, brain imaging studies reveal that some people affected by autism show higher than normal activity in brain regions associated with social behavior.
This latest experimental evidence further suggests that restoring balance to brain activity may be a way to relieve some of autism’s core symptoms. It also provides groundwork for future research investigating the role that specific brain circuits play in autism. Deisseroth and his colleagues are already developing new mouse models that will allow scientists to manipulate the activity of other brain regions and circuits, promising a more precise picture of how brain signaling problems might give rise to autism’s core symptoms.
Yizhar O, Fenno LE, Prigge M, et al. Neocortical excitation/inhibition balance in information processing and social dysfunction. Nature. 2011 July 27;477(7363):171-8.