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Identification of biomarkers to slow neurodegenerative diseases

Updated: Oct 19, 2023

The opening scene in the movie Déjà Vu (2006) shows a New Orleans ferry explode killing 543 people, the result of a domestic terrorist. Special Agent Carlin (Denzel Washington) investigates the bombing and taps into Snow White, a surveillance program that uses previous satellite footage to form triangulated images of events four-and-a-half days in the past. The genre isn’t a drama, it is a sci fi; Snow White is actually a time window that is exploited by Carlin to travel back in time to save the ferry passengers. Predictably, any tweak Carlin makes during his time travel permeates opening a multiverse of possibilities while collapsing others. In Hollywood’s twisted interpretation of time travel, all live happily after.

How does Déjà Vu relate to the conundrum of the by-stander mechanism of equine polyneuropathy and complex neurodegenerative diseases in people? We explained by-stander responses in a previous blog. Use the link to review the by-stander mechanism. To summarize, the inciting cause is long gone but the innate pro-inflammatory responses continue in a chronic inflammatory state.

Complex human diseases include Amyotrophic Lateral Sclerosis (ALS), Parkinson’s Disease (PD), and Alzheimer’s Disease (AD. A lingering question is what risk factors in an individual drive pathology to one disease over another? Is there an explanation of commonality of exposure or risk? Is there a gene that makes one disease prevail? Is there a genetic bias of a sensitive receptor in tissue neurons specific to an individual that selects one disease in preference to the other diseases? A single point mutation in a receptor perhaps. Remember, these diseases are pluricausal (many causes) and causal factors are pleotropic (they cause more than one disease). Diagnosing the cause of disease requires a list of disease triggers and individual risk factors. Non-single-gene complex diseases are pluricausal and caused by different pathogenic factors present in the population with no single cause responsible for more than a few percent of ALS, PD, or AD.

It is tempting to isolate and induce specific cells (induced neuron-like cells for ALS, basal cells from the substantia nigra for PD, and astrocytes from the frontal and temporal lobes of the brain for AD) and look for markers that are common between the patients suffering from the disease. Researchers know that cells isolated and tested in vitro do not behave as they did in the whole organism. The organism is an interaction of many cell types, thus a monoculture of cells can’t reproduce the interaction of a cells on neurons in the nervous system. To summarize, each response in an individual initiates cascading reactions that simultaneously collapse other pathways tipping the balance of a disease to a phenotype, if any. These are rare diseases, as more toxins are present in the environment these diseases will become more common. A common theme is mishandled toxic proteins, different for each neurodegenerative disease.

Our goal is to develop a surveillance system (biomarkers) and image the results of immune events that happened days or months prior, thus mapping an individual’s innate multiverse, and given enough data from ALS, PD or AD cases perhaps we could predict personalized therapeutic targets. We already do this with polyneuritis, that is what our biomarker testing panel and our field trial are about. We want to develop an AI analysis of metabolomic data from a simple blood sample to analyze and map 2000 disease-relevant phosphokinase sites— and their interactions, for human neurodegenerative diseases. It is a look back in time that will hopefully change a patients future. Perhaps we will call the project Snow White. The science we generate will be applicable to horses in the near future.



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