There's growing evidence that the underlying cause of dementia is not the beta amyloid proteins that then develop into plaques that can interfere within neurons communicating efficiently. New thinking by Rudy Tanzi and Robert Moir and others now suggests that amyloid activity is part of the earliest forms of our immune system. Our work with neurofeedback and photobiomodulation supports this way of thinking as it refocuses attention at the system level where many factors can be considered 'causal' in the deterioration of synaptic communication. This leads to thinking more broadly and creatively about intervention strategies that include non-drug, noninvasive technologies like neurofeedback and infrared light therapy. The following discussion provides a context for how they arrived at this new view of beta amyloid as not the primal generator in neurodegeneration.
Our team regularly publishes articles and blog posts on the latest research and news coming out of our group and the field in general.