Quietmind Foundation

The etiology of Alzheimer's dementia is, at best multifactorial. Before the emergence of cognitive impairment, symptoms such as thinning of the cortex, accumulation of β-amyloid, and decreased hippocampal volume are common. Hence, the accumulation of β-amyloid and hyperphosphorylated tau fibrillary tangles are two pathological hallmarks in Alzheimer's disease brains, but antibody therapy aimed to decrease β-amyloid has been a failure and, in most optimistic opinions, may delay somewhat disease progression. However, 31-38 % of subjects develop cerebral micro-hemorrhages in aducanumab therapy, an antibody to the amyloid beta plaque by Biogen. Genetics such as Apo E3/E3 have demonstrated defects in the blood-brain barrier in early-onset dementia. Late Onset Alzheimer’s Dementia, has implicated microbe cerebral infections and numerous genetic single nucleotide polymorphisms. However, several cellular biological signatures of Alzheimer's disease have been identified, such as synaptic dysfunction, β-amyloid plaques, hyperphosphorylated tau, cofilin-actin rods, and Hirano bodies which are related to the actin cytoskeleton. Cofilin is one of the most affluent and common actin-binding proteins and plays a role in cell motility, migration, shape, and metabolism. They also play an important role in severing actin filament, nucleating, depolymerizing, and bundling activities. This review summarizes the structure of cofilins appearing after ATP interruptions and deficits in mitochondrial and microtubules and their functional and regulating roles, focusing on the synaptic dysfunction, β-amyloid plaques, hyperphosphorylated tau, cofilin-actin rods, and Hirano bodies of Alzheimer's disease. These findings strengthen our hypothesis that Alzheimer’s dementia is characterized by “Quantum Decoherence” resulting from mitochondrial and microtubular deterioration and responding to near-infrared transcranial photobiomodulation to support mitochondrial and microtubule repair, regrowth and neuronal synaptic renormalization.

treatment group 53.0%(97) of subjects or lost1kg/m. In the control group, 55.6%(25) of subjects gained or lost1kg/m. The change in BMI between treatment group and controls did not differ significantly after 1 year. Anecdotally, some of the subjects according to the authors initially lost weight after starting CPAP but eventually gained it back 1 year later. 181 patients with obesity and C-reactive protein (CRP) greater than 1.0mg/liter were randomized to CPAP, a weight-loss intervention, or CPAP plus weight loss intervention for 24 weeks. The results in 146 participants with a reduction in CRP levels, insulin resistance and serum triglyceride levels in those assigned to weight loss only and to the combined interventions, but not in the CPAP alone group. BMI did not significantly decrease in any group treated with CPAP. 2

Evidence from animal and human studies regarding the biological impact of near infrared light stimulation has significantly increased of late noting the disease modifying properties of photobiomodulation for improving physical and cognitive performance in subjects with a variety of neurodegenerative conditions. Concurrently we see a growing body of literature regarding the efficacy of operant conditioning of EEG amplitude and connectivity in remediating both cognitive and behavioral symptoms of both neuropsychiatric and neurodegenerative disorders including traumatic brain injury, ADHD, PTSD, and dementia. This presentation seeks to outline a treatment model combining these two treatment methods to stop the progression of neurodegeneration using pulsed (10hz), brief (5-20minutes) repeated (1-2x/daily) transcranial and intranasal photobiomodulation with 810nm and 1068nm near infrared phototherapy and operant conditioning of EEG amplitude and coherence. Our initial study on treating dementia with EEG biofeedback (N=37) showed neuroplasticity's potential for modifying cognitive and behavioral symptoms using the evidence from decades of neurological research that never felt the warm touch of a translational researcher's hand. The near infrared interventional studies clarified the order of treatment, i.e., tissue health and renewal were achieved, followed by neural connectivity enhancement. Significant improvements in both immediate and delayed recall and praxis memory as well as executive functioning and behavioral regulation were obtained with each intervention. The inferred synergistic impact of properly combining these approaches is what informs our current clinical applications and future research efforts examining the value of combined treatments for all dementias, parkinson’s disease and age-related dry macular degeneration.