Relationship between susceptibility to neurodegenerative diseases and genetic factors in populations exposed to mercury in Medellín, Colombia.

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a recently defined inflammatory demyelinating disease of the central nervous system (CNS). The clinical course of MOGAD can be either monophasic or relapsing and it has the potential for long-term neurological disability. The diagnostic criteria require the presence of the MOG antibody and at least one core clinical demyelinating event of optic neuritis, myelitis, acute disseminated encephalomyelitis (ADEM), cerebral monofocal/polyfocal deficits, brainstem or cerebellar deficits, or cerebral cortical encephalitis. In children, ADEM and optic neuritis are the most common presentations while in adults optic neuritis predominates. Psychiatric disorders, with depression as the most common, are the leading contributor in morbidity and socioeconomic burden in the USA. In other demyelinating diseases of the CNS such as multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) with aquaporin-4 antibodies (AQP4-IgG), psychiatric comorbidities are highly prevalent, with depression and anxiety occurring in approximately 24–54% of patients with MS and other studies suggesting similarly high rates in NMOSD. Psychiatric comorbidities in MS have been associated with diagnostic delay, higher relapse frequency, reduced treatment adherence and worse clinical outcomes, including disability worsening and fatigue. Given the shared clinical and pathobiological features of MOGAD, MS and NMOSD – including acute immune-mediated attacks of CNS inflammatory demyelination and comparable burden of acute neurological disability – a similar psychological burden in MOGAD patients seems plausible. However, in contrast to MS, the relevance of psychiatric comorbidities in MOGAD – their frequency, clinical spectrum, and onset – remain unclear.