6th Edition of Neurology World Conference 2026

Abstract

Abstract
Attenuation of Beta-Amyloids and Other Risk Factors by a Micronutrient Mixture of Probiotics, Collagen Peptides, Omega 3, and CBD in Alzheimer’s Disease. Kedar N. Prasad, Engage Global, Inc., 245 El Faisan Drive, San Rafael, California 94903.
During the last decades, several endogenous risk factors that participate in the development and progression of Alzheimer’s disease (AD) have been identified. They include increased oxidative stress, chronic neuroinflammation, mitochondrial dysfunction, autophagic dysfunction, progressive loss of acetylcholine, oxidation of omega-3 fatty acids, increased production of beta-amyloids, hyperphosphorylation of tau protein, loss of collagen, and intestinal dysbiosis. Among these risk factors, beta-amyloids have drawn significant attention from neuroscientists and neurologists. Using beta-amyloids as a target, antibodies have been developed for the treatment of AD. These anti-amyloid antibodies have serious side effects and produce only a short-term benefit in patients with early-phase AD. Another risk factor involves a gradual decline in the levels of acetylcholine. To address this, drugs that increase the levels of acetylcholine in the cholinergic neurons by inhibiting acetylcholinesterase were developed. The effectiveness of these drugs depends on the viability of neurons. Since they do not address the cause of neuronal death, the beneficial effects of these drugs last only for a few months. Neither anti-beta-amyloid antibodies nor acetylcholinesterase inhibitors have any role in the prevention of AD. This review proposes a prevention plan for AD that addresses all endogenous risk factors, including beta-amyloids, at the same time. This plan involves supplementation with a micronutrient mixture, probiotics with prebiotics, collagen peptides, and omega 3. It also suggests that combining drugs with the prevention plan together with CBD (cannabidiol) may prolong the effectiveness of drugs, improve behavior abnormalities associated with AD, and possibly reduce the potential toxicity of drugs.