Just like the long-term impact of age and chronic exposure to environmental factors can affect our health, the consequences of a ticking clock and persistent challenges can create lasting effects on our lives. As we grow older, the prevalence and costs of neurological conditions, such as Alzheimer’s Disease, are on the rise. One intriguing hypothesis suggests that the detrimental effects of environmental risk factors may be linked to an accelerated biological age. This theory gains support from studies showing that dietary restriction, which delays age-related diseases, also mitigates the harmful impacts of environmental factors. Both age and environmental risks result in the accumulation of mutations and modifications that reflect our ‘biological age’—a better predictor of age-related ailments than our actual years on this planet. The research examines the influence of environmental risk factors like smoking and air pollution on neurological conditions by hastening our biological clock through persistent epigenetic changes and somatic mutations. By unraveling these mechanisms, we could potentially develop interventions that prolong the damaging effects of both aging and environmental risks. To dive deeper into the fascinating findings, check out the full article!

Since the development of antibiotics and vaccination, as well as major improvements in public hygiene, the main risk factors for morbidity and mortality are age and chronic exposure to environmental factors, both of which can interact with genetic predispositions. As the average age of the population increases, the prevalence and costs of chronic diseases, especially neurological conditions, are rapidly increasing. The deleterious effects of age and environmental risk factors, develop chronically over relatively long periods of time, in contrast to the relatively rapid deleterious effects of infectious diseases or accidents. Of particular interest is the hypothesis that the deleterious effects of environmental factors may be mediated by acceleration of biological age. This hypothesis is supported by evidence that dietary restriction, which universally delays age-related diseases, also ameliorates deleterious effects of environmental factors. Conversely, both age and environmental risk factors are associated with the accumulation of somatic mutations in mitotic cells and epigenetic modifications that are a measure of “biological age”, a better predictor of age-related morbidity and mortality than chronological age. Here we review evidence that environmental risk factors such as smoking and air pollution may also drive neurological conditions, including Alzheimer’s Disease, by the acceleration of biological age, mediated by cumulative and persistent epigenetic effects as well as somatic mutations. Elucidation of such mechanisms could plausibly allow the development of interventions which delay deleterious effects of both aging and environmental risk factors.

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