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Multiple sclerosis (MS) is a chronic multifaceted demyelinating and neurodegenerative disease of the central nervous system (CNS) of presumed autoimmune origin.1
Patients with MS are characterised by a spatial and temporal dissemination of neurological sign and symptoms, by the presence of multifocal lesions in the periventricular white matter on MRI scans and by an immunoglobulin synthesis within the CNS.1 Further diagnostic tools are desirable, and the use of blood and cerebrospinal fluid (CSF) biomarkers may contribute to the comprehension of the disease’s pathogenesis and progression.
Autophagy is an evolutionarily conserved and genetically controlled cellular process where intracellular components are sequestered within double-membrane vesicles (autophagosomes), which then fuse with lysosomes where the material is degraded.2 Autophagy also occurs as mitophagy, which is responsible for the removal of aberrant, aged and wasted mitochondria. Interestingly, autophagic/mitophagic pathways have been found deregulated in various human diseases. In particular, it has been demonstrated how these catabolic pathways are implicated in several neurodegenerative diseases such Alzheimer’s and Parkinson’s diseases and amyotrophic lateral sclerosis.2 Moreover, recent studies suggest a role of mitochondrial dysfunction in the neurodegenerative aspects of MS.3 Despite these observations, the role of autophagy and mitophagy in MS is still elusive.
To tackle the question, we tried to verify the frequency of specific autophagic markers (ATG5 protein) and mitophagic markers (Parkin protein) in patients with MS and in neurological controls.
Forty consecutive untreated patients with relapsing–remitting MS (RRMS) were included in the study (24 women and 16 men; mean age=40.7±10.5). Forty patients with other inflammatory neurological diseases (OINDs) (21 women and 19 men; mean age=55.9±17.5) and 40 subjects with …
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