Abstract
A three-part mechanism is proposed for the induction of Alzheimer’s disease: (1) decreased blood lactic acid; (2) increased blood ceramide and adipokines; (3) decreased blood folic acid. The age-related nature of these mechanisms comes from age-associated decreased muscle mass, increased visceral fat and changes in diet. This mechanism also explains why many people do not develop Alzheimer’s disease. Simple changes in lifestyle and diet can prevent Alzheimer’s disease. Alzheimer’s disease is caused by a cascade of events that culminates in damage to the blood–brain barrier and damage to neurons. The blood–brain barrier keeps toxic molecules out of the brain and retains essential molecules in the brain. Lactic acid is a nutrient to the brain and is produced by exercise. Damage to endothelial cells and pericytes by inadequate lactic acid leads to blood–brain barrier damage and brain damage. Inadequate folate intake and oxidative stress induced by activation of transient receptor potential cation channels and endothelial nitric oxide synthase damage the blood–brain barrier. NAD depletion due to inadequate intake of nicotinamide and alterations in the kynurenine pathway damages neurons. Changes in microRNA levels may be the terminal events that cause neuronal death leading to Alzheimer’s disease. A new mechanism of Alzheimer’s disease induction is presented involving lactic acid, ceramide, IL-1β, tumor necrosis factor α, folate, nicotinamide, kynurenine metabolites and microRNA.
Highlights
The age-related nature of these mechanisms comes from age-associated decreased muscle mass, increased visceral fat and changes in diet
As many Scientists have published for many years, amyloid β and tau are not the causes of Alzheimer’s disease
The variables that are common to all these risk factors are sedentary lifestyles and visceral fat obesity
Summary
The failure of anti-amyloid β therapies in the treatment of Alzheimer’s disease [1,2,3,4,5]. Decreased blood lactic acid is involved in causing Alzheimer’s disease. Lactic acid is an energy source for brain neurons, astrocytes and pericytes [15] It is taken up across the blood–brain barrier and into cells by anion channels and monocarboxylic acid transporters [16]. Due to sarcopenia and sedentary lifestyles, many people may not get enough lactic acid to supply essential energy to brain cells, especially cells of the blood–brain barrier. Damage to pericytes and the blood–brain barrier are prominent features of Alzheimer’s disease [25]. Inadequate inhibition of TRPV1 by low levels of lactic acid causes pericytes to die. Exercising muscles secrete myokines into the blood These proteins have a number of beneficial functions in the brain and the blood–brain barrier. At low levels enhances brain-protective mechanisms, at high levels damages DNA and other macromolecules
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