Cell-Specific Aging in Multiple Sclerosis

The deleterious effects of aging on health are well recognized across all organ systems. In neurology, age is associated with Alzheimer disease, Parkinson disease, stroke, and the neurodegenerative treatment refractory form of multiple sclerosis (MS), traditionally described as progressive MS. As people with MS age, their odds of having acute attacks decline and they are more likely to steadily accumulate neuronal damage and disability. Rather than a separate category of disease, progressive MS is most likely a result of "host" factors affecting the underlying autoimmune pathophysiology. These host factors include age, sex, environmental exposures including smoking, and genetic factors. With current evidence, the strongest of these is age. The association of chronological age with accumulation of ambulatory disability is one of the most highly replicated results in observational studies of MS.1 More recently, efforts have been made to better define this association by measuring an individual's biological age. Individuals with the same birthdate may have competing protective and deleterious factors affecting their overall resilience to aging processes, such as oxidative stress and DNA damage. By estimating true biological age, we may more precisely be able to elucidate how age drives progressive disease and design effective interventions for relevant aging pathways.