A Molecular Mechanism of Stress-Induced Alzheimer's Disease; Part 1

Alzheimer's disease (AD) is a chronic but deadly neurodegenerative disorder. A significant burden on global public health, a cure for AD is still elusive. Recent clinical trials based on pathogenic theories of extra/intracellular protein aggregation resulting from oxidative stress or other environmental insults have encountered setbacks. In this first part of a series, we report a significant and serendipitous case of an AD patient. It is the first time, to our knowledge, to follow a single patient over 33 plus years (1985-2018), where AD symptoms were presented and remised repeatedly. The effects of stress resulting in numerous ailments, e.g., memory loss, brain atrophy, high blood pressure, inflammations, decrease of immunity, etc., were observed in four 'episodes' of severe stress, confirming that the disease is stress-induced. An anti-stress lifestyle, involving seven daily anti-stress practices, was implemented which, remarkably, led to the recovery of memory and retardation of disease progression. We discovered a relationship between stress/stress hormones, the strain effects on these stress hormones and the pathways leading to a stress-induced macro-molecular mechanism that accounts for the origin of toxic free radical species (oxidants) which derive from Amyloid beta (A & beta;) and Tau proteins (antioxidants). We suggest our mechanism may also be applied to other neurodegenerative diseases related to stress effects on proteins, such as alpha-synuclein in Parkinson's disease, superoxide dismutase in amyotrophic lateral sclerosis, IAPP amyloid in type 2 diabetes, etc. As chronic traumatic encephalopathy and post-traumatic stress disorder both lead to AD, the anti-stress program proposed here may also very well be of assistance to those impacted by the said ailments described above. Consequently, the proposed stress-induced molecular mechanism deduced from the Alzheimer disease patient's experience, we suggest, represents a significant step forward in understanding the origins of Alzheimer's disease and many other neurodegenerative diseases. In part 2, we will discuss the patients further AD development from 2018 to the current-time and expand our discussion of the physics of stress/strain on the macromolecules.