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Introduction: Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS) characterized by T-cell-mediated autoinflammation and demyelination of neurons with its typical presentation in young adulthood. Adverse childhood experiences (ACEs) are proposed to increase the risk of developing multiple sclerosis (MS) later...
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... Both epidemiological and experimental studies have found an association between adverse childhood experiences (ACEs) and MS [19][20][21][22][23]. ACEs represent potentially traumatic events, such as abuse or neglect, witnessing violence, or growing up in a household with drug use, mental health problems, or instability due to parental separation, death, or incarceration. ...
... Two systematic reviews have summarized the evidence from observational studies investigating the association between ACEs and MS [19,21]. The systematic reviews investigated MS onset and other clinical features of MS in association with ACEs. ...
... Both reviews concluded that the evidence supports a link between childhood stress and MS risk. They also reported that people with a history of ACEs develop MS symptoms at a younger age, that they have more fatigue and exaggerated reaction to pain, and that ACE severity is associated with an increased rate of MS relapses [19,21]. ...
Adverse childhood experiences (ACEs), such as abuse, neglect, and household dysfunction, contribute to long-term systemic toxic stress and inflammation that may last well into adulthood. Such early-life stressors have been associated with increased susceptibility to multiple sclerosis (MS) in observational studies and with the development of experimental autoimmune encephalomyelitis in animal models. In this review, we summarize the evidence for an ACE-mediated increase in MS risk, as well as the potential mechanisms for this association. ACEs dysregulate neurodevelopment, stress responses, and immune reactivity; they also alter the interplay between the immune system and neural networks. All of this may be relevant for MS risk. We further discuss how ACEs induce epigenetic changes and how the toxic stress caused by ACEs may reactivate the Epstein-Barr Virus (EBV), a key risk factor for MS. We conclude by suggesting new initiatives to obtain further insights into this topic.
