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Autophagy and mitophagy elements are increased in body fluids of multiple sclerosis-affected individuals
  1. Simone Patergnani1,
  2. Massimiliano Castellazzi2,
  3. Massimo Bonora1,
  4. Saverio Marchi1,
  5. Ilaria Casetta2,
  6. Maura Pugliatti2,
  7. Carlotta Giorgi1,
  8. Enrico Granieri2,
  9. Paolo Pinton1
  1. 1 Department of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy
  2. 2 Department of Biomedical and Specialist Surgical Sciences, Section of Neurological, Psychiatric and Psychological Sciences, University of Ferrara, Ferrara, Italy
  1. Correspondence to Professor Paolo Pinton; paolo.pinton{at}

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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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  • SP and MC contributed equally.

  • Contributors SP, CG, EG and PP conceived and designed the experiments. SP and MC conducted the experiments, analysis of samples, analysis and interpretation of data. MB, SM, MP and IC helped with patients’ enrolment and data analysis. SP, MC, EG and PP wrote the manuscript. All authors have reviewed and approved the content and submission of this manuscript.

  • Disclaimer Since this article has been published the author name Ilaria Casetta has been updated.

  • Competing interests None declared.

  • Patient consent Obtained.

  • Ethics approval The Committee for Medical Ethics in Research of the University of Ferrara.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Correction notice Since this article has been published the author name Ilaria Casetta has been updated.