What is it about?
The molecular and cellular data on Alzheimer's disease and neurotoxicity that are available in the public domain were structured according to key events describing toxic tau-protein mediated memory loss. Neurotoxic environmental compounds were found to be able to plug into Alzheimer's disease relevant processes. Over 20 molecular initiating events affecting Alzheimer's disease initiation and early development were identified.
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Why is it important?
While over the years mechanistic data have been produced describing the clinical phase of early onset Alzheimer's disease, little is still known about the early (non-clinical) phases of late onset Alzheimer's disease. While aging and genetics play a role in late-onset Alzheimer's disease, evidence strongly suggests that environmental and systemic risk factors play an important role. The collected and structures data identified the toxic tau-protein driven adverse pathway as a plausible pathway towards memory loss. From the collected data it was also clear that this pathway is only one of a network of pathways that contribute to late-onset Alzheimer's disease initiation and development.
Perspectives
The proposed tau-driven adverse pathway is to stimulate the development of other adverse pathways and to build a network of adverse pathways driving late-onset Alzheimer's disease. Understanding the early preclinical processes driving initiation and progression towards clinical late-onset Alzheimer's disease, is anticipated to open up for the development of diagnostic tools , and eventually drugs, targeting adverse events occurring before irreversible brain damage occurs. Eventually, this will be at the benefit of the patients and their families.
Dr. Erwin L J Roggen
ToxGenSolutions BV
Read the Original
This page is a summary of: A Tau-Driven Adverse Outcome Pathway Blueprint Toward Memory Loss in Sporadic (Late-Onset) Alzheimer’s Disease with Plausible Molecular Initiating Event Plug-Ins for Environmental Neurotoxicants, Journal of Alzheimer s Disease, May 2021, IOS Press,
DOI: 10.3233/jad-201418.
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