September 18-20, 2021 | New York Hilton, NY

Genes vs Environment in Alzheimer’s Disease

Sep 18 2021
2:00 pm - 3:15 pm
Aristo Vojdani, PhD, MSc, CLS

Like many autoimmune diseases, the etiology of Alzheimer’s disease (AD) is due to a combination of genetic predisposition and environmental factors that alter the expression of immune regulatory genes through various mechanisms. Both cellular and humoral response against different components of the brain plus other inflammatory molecules contribute to amyloid-β plaque formation, which is the hallmark of AD. Although for many years environmental factors such as pathogens and toxic chemicals had been associated with AD, no direct evidence had been presented for the specific role of these factors in amyloidogenesis. In search of such a mechanism, we engaged in research that resulted in the publication of three different manuscripts in 2018. In the first of these three articles, we used a specific monoclonal antibody made against Aβ42 which not only reacted strongly with Aβ42, tau protein and α-synuclein, but also had from weak to strong reactions with 25 different pathogens or their molecules, some of which have been associated with AD. We also found that bacterial molecules from infectious pathogens can bind to AβP, forming the amyloid plaques that are the tell-tale markers of Alzheimer’s disease. In the second of the three articles, our results indicated that reaction between AβP-42 antibody with specific chemicals bound to HSA and numerous food antigens might play a role in AD. In the third article, we found that the same AβP-42 antibody also reacted with neural proteins involved in AD and growth factors that play important roles in neural regeneration and repair. Our third study also showed that although the levels are much higher in patients with Alzheimer’s disease, antibodies to these neural proteins, toxic chemicals and reactive foods are also found in healthy subjects; in individuals with compromised BBBs these antibodies that cross-react with AßP-42 can reach the brain, where their cross-reactivity with AßP-42 may contribute to the onset and progression of AD, and perhaps other neurodegenerative disorders. However, due to the unique and individualistic nature of the human being, not all human beings will have the same immune response. A person’s unique genetic makeup, the composition of his microbiome, the environmental factors that surround him from pre-birth to maturity, his personal diet, habits and lifestyle all ensure that every individual has a personalized immune system that is different from someone else’s. That is why it is necessary to have a personalized antibody detection system (PADS) that tests for a group of antibodies that are produced by the immune system of an individual against a set of environmental triggers (pathogens, foods and toxic chemicals) that the individual’s body cannot tolerate. These specific antibodies have the potential to become disease-specific if they cross-react with particular tissue antigens involved in different autoimmune diseases. At the very early stage of autoimmunities, including Alzheimer’s disease, these detected antibodies may not be pathogenic. However, later on, if these antibodies penetrate to the targeted tissue antigens, they may contribute to the progression of many autoimmune diseases. Among the population, individual differences exist in the production of antibodies against multiple antigens that are associated with Alzheimer’s disease. Detection of antibodies against polyantigens give a clear warning about epigenetic propensities and the need for clear intervention based on the individual’s personalized antibody immune print. If these triggers are removed based on the PADS, the reduction of the blood level of antibodies may enable practitioners to prevent the progression of autoimmune diseases, including Alzheimer’s disease. PADS is the best guide for identifying the triggers first, then removing the triggers, followed by repairing the barriers to prevent Alzheimer’s and other neurodegenerative disorders.

Learning Objectives:
  1. Demonstrate how genes actually play a minimal role in Alzheimer’s disease and why environment is a major factor.
  2. Observe how Alzheimer’s disease is a slow-burning disease, and because of the gradual development and the role of the environment, a unique window of opportunity exists for intervention.
  3. Show how antibodies to these various environmental factors can be found in both healthy individuals and patients with Alzheimer’s disease, but are found in much higher levels in those suffering from the disease.
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