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The average age of people with MS is increasing, but knowledge of the disease in people over age 55 remains sparse.
Abedallah A. K. Balusha, MD, and Sarah A. Morrow, MD, MS, FRCPC, FAAN
Historically, MS was recognized as a disease of young people as the typical onset is between age 20 to 40 years.2 The life expectancy of the general population, however, is increasing. Additionally, advances in MS treatment have led to an increase in the average age of persons with MS.3 Thus, MS can no longer be considered a disease of earlier adulthood only because clinicians will be treating people with MS into their later decades of life. Simultaneous management of aging and MS is among the current unmet needs in MS care, considering the unclear phenotypes, disease course, associated comorbidities, aging of the immune system (immunosenescence), MRI characteristics, response to disease-modifying therapies (DMTs), and disease progression. In this review, we address several issues pertinent to the care of people with MS in a person’s mid50s and beyond, discussing the epidemiology of MS in this population, immunosenescence, use of DMTs, and, finally, cognitive impairment.
EPIDEMIOLOGY OF MS AFTER AGE 55
Multiple sclerosis affects persons of all ages. Age is a predictor of MS phenotypes and onset of relapsing MS (RMS) between age 20 to 40 years accounts for 80% of cases. Secondary progressive MS (SPMS) is considered the long-term outcome of RMS, but more than 30% of people with MS continue to have RMS at an advanced age.4 Only 3.4% of people with MS are diagnosed with RMS after age 50, considered late-onset MS, and only 1% are diagnosed after the age 60, considered very late-onset MS.2
In contrast, the primary progressive MS (PPMS) phenotype tends to present after age 45 and accounts for 10% to 15% of cases. PPMS is characterized by a slow neurologic decline from onset.5 Yet, the overall demographics of people with MS are changing to include people in their mid50s and later. For example, in Manitoba, Canada, the reported prevalence of MS has increased from 32.6 per 100,000 in 1984 to 226 per 100,000 in 2006, with evidence of increased age of peak prevalence from 35 to 39 years to 55 to 59 years.6 Similarly, in Italy, 18% of people with MS are age 65 or more.7 Thus, the care of people age 55 and more is becoming part of routine practice in MS clinics. Whether people with MS who first present later in life have a different phenotype is not yet well studied.
IMMUNOSENESCENCE
Aging is well known to be associated with progressive loss of innate and adaptive immune system proficiency and an adequate immune response (immunosenescence). These changes have many implications for people with MS.8 It has been suggested that there are 2 parallel inflammatory processes during the course of MS that manifest as the relapsing and progressive MS phenotypes. In simple terms, the first is invasion of the brain by T and B lymphocytes through a blood-brain barrier damaged by inflammation, presenting as clinical relapses and active demyelination. The second is a slow accumulation of B and T cells in the meninges without major blood-brain-barrier breakdown, forming aggregate or lymphoid follicles, which cause a slow inflammatory process and neurodegeneration, resulting in a progressive phenotype. These latter changes may present early in the course of MS but become more predominant at late stages.9
In the early stages of MS, typically occurring at age 20 to 40 years, the immune system is more functional, with repair capacity that is more effective in healing the inflammatory damage. With aging, the immune system repair capacity decreases, and axonal degeneration, iron deposition, and oxidative stress occur, leading to decreased natural brain reserve. This gradual decrease in healing and brain reserve might partly explain the progression of MS seen with aging.10 The difference between the immune response in the early stage of RMS compared with progressive MS may also explain why evidence of reduced disability and disease progression has not been shown for most DMTs, based on probable different mechanisms of disease activity for relapse vs progression.11
READ COMPLETE ARTICLE, HERE (from The Neurology Hub)
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