A newly formed cross-disciplinary consortium is set to advance studies in epigenetics, mechanobiology, and environmental toxicology, focusing on crucial issues like arsenic remediation in groundwater and mechanotransduction in Alzheimer's and cancer. The collaborative effort arises from a unified academic momentum, underscoring the interconnectedness of environmental factors and disease mechanisms, with the goal of securing additional funding and disseminating impactful results. This strategic initiative aims to leverage recent research enthusiasm to drive significant advancements in addressing the dual crises of neurodegenerative diseases and environmental health.
“Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder worldwide and the leading cause of dementia, accounting for more than two-thirds of cases.”
“Epidemiological projections estimate that the global prevalence of AD will triple by 2050, exceeding 91 million cases, with annual economic costs surpassing USD 1 trillion.”
“Clinically, AD is classified into early-onset Alzheimer’s disease (EOAD), which represents less than 5% of cases and manifests before the age of 65.”
“In contrast, LOAD arises from complex interactions between genetic susceptibility—most notably the APOE ε4 allele—and diverse environmental and lifestyle factors.”
“mutations in APP or in the presenilin genes (PSEN1 and PSEN2) favor Aβ42 production and lead to familial, early-onset AD.”
“In contrast, sporadic late-onset AD shows no single genetic cause, redirecting attention toward epigenetic mechanisms.”
“Overall, DNAm serves as a molecular link between environment, lifestyle, and disease progression.”
“Several studies report hypomethylation of the APP promoter in AD brains, which often correlates with elevated APP expression and greater Aβ burden.”
“Folate and B12 deficiencies have been strongly linked to hypomethylation of APP and presenilin promoters in both human and animal models.”
“Maternal dietary choline supplementation in AD mouse models has been shown to improve the disease phenotype, reducing Aβ plaque accumulation.”
“For example, adherence to a Mediterranean diet reduces risk by 11–30% in human cohorts.”
“It has also been shown in human studies that the Mediterranean Diet reduces the risk of developing AD, probably due to changes in the epigenetic marks.”
