AbstractBackgroundPresence Environmentally Mediated Intellectual Decline Neurotoxins ('presence‐EMIDN') threats from 'bounded', 'unbounded' and 'pervasive' sources puts everyone at risk of developing neurodegenerative diseases (eg. Alzheimer) once specific lipophilic‐neurotoxins breach the blood‐brain and nose‐brain barriers to reach the brain and build up to harmful thresholds. Such neurotoxins exist; how they provoke Wallerian‐type degeneration to cause FAD have been threaded together from experimental evidenced‐based reviews. My intent/interest is to create awareness and establish the aetiology for FAD, which has remained idiopathic since 1906, when the German Neurologist, Alois Alzheimer, discovered the disease.MethodThrough threaded literature reviews from multiple sourcesResultsMany neurotoxins produce Wallerian‐type degeneration: organophosphorus compounds (DFP, TOCP), acrylamide, n‐hexane and some of its metabolites. Wallerian‐type degeneration have been demonstrated in animals: hens, cats, rats, rabbits. Changes during Wallerian‐type degeneration can be grouped into two (Histopathological and Biochemical): it describes the cascade of events taking place in the distal part of an axon that has been cut or crushed. The histopathological changes occur in stages in the following order of succession: stage a: primary degeneration of axon followed by secondary degeneration of myelin in these order: axon swelling; axon disintegration; loss of normal myelin structures with swelling; tumefaction; and breakdown of myelin sheaths; followed by stage b: Cellular proliferation; and then stage c: Fibrosis. The biochemical changes result from liberations of normal biochemical constituents of axon and myelin. There is specifically a decrease in the CNS neurotransmitter's Acetylcholine content, in stage a (causing deficiency‐imbalance), increase in collagen in stage c, and other stage b changes.ConclusionThere are evidences showing that symptoms of FAD is due to 'Acetylcholine deficiency‐imbalance in the brain' where it exercises Excitatory and Inhibitory effects which progressively kick‐starts FAD with fatalities after 5 years. Establishing this aetiology brings vistas of new hope/challenges for possible therapeutic interventions developments.
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