Professor Larry Reid, RPI, Cognitive Science

 

Professor Larry Reid, RPI, Cognitive Science

Sage 4101

October 26, 2016 12:00 PM - 1:30 PM

The hypothesis is that Alzheimer disease (AD) is (a) a reduction in the efficiency of the regular clearance of excess amyloid beta (Aβ) which sets the initial stages of the progressive disease that is AD; (b) further, that the initial events of many instances of AD begin with ill-health at the brain-nasal cavity (B-NC) interface; (c) disease of the B-NC interface hinders olfactory perception and disrupts the flow of fluids from the medial temporal pole to the cervical lymphatics; (d) that flow of fluids sustains the homeostasis of the anterior olfactory nucleus, piriform and entorhinal cortices, and eventually, the hippocampus and related areas, areas that are progressively unhealthy during the initial and middle stages of AD; (e) therefore, preventing and treating any dysfunction of fluid flow from the medial temporal pole at the B-NC interface will prevent and treat early stages of AD; (f) treating lost olfactory perception and disturbances of sleep will improve fluids flowing from the brain at the B-NC interface, thereby restoring homeostasis in the limbic system, and thereby treating early stages of AD; and (g) the most efficient way of treating lost olfaction and sleep disturbances is by way of behavioral therapy.  In this review with hypotheses, these points will be addressed leading to implications of how behavioral therapies, or training, aimed at olfaction, sleep, exercise and practicing specially designed computer-assisted game-like programs may be a feasible avenue toward reducing Alzheimer’s disease risk and morbidity.

 

Download the paper here. 

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