Mitochondria in Multiple Sclerosis: Molecular Mechanisms of Pathogenesis

Patergnani, Simone; Fossati, Valentina; Bonora, Massimo; Giorgi, Carlotta; Marchi, Saverio; Missiroli, Sonia; Rusielewicz, Tom; Wieckowski, Mariusz R.; Pinton, Paolo

doi:10.1016/bs.ircmb.2016.08.003

Cited by 71 publications

(53 citation statements)

References 272 publications

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“…Notably, local sterile inflammation has been shown to be finely linked with the development and the progression of different NDDs, such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) [65,66]. Neuroinflammation is commonly driven through the abnormal activation of brain immune cells, namely, microglia and astrocytes, by DAMP molecules released from damaged and necrotic cells [67,68].…”

Section: Role Of Mitochondria and Neuroinflammation In Neurodegeneratmentioning

confidence: 99%

“…Necroptosis can be stimulated by TNF, other members of the TNF death ligand family, interferons, Toll-like receptor signaling and viral infection [105]. In MS patients, the RIPK1-RIPK3-MLKL pathway is activated, and experiments in animal models showed that oligodendrocytes necroptosis could be blocked by RIPK1 inhibition [66,106].…”

Section: Role Of Mitochondria and Neuroinflammation In Neurodegeneratmentioning

confidence: 99%

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The Role of Mitochondria in Inflammation: From Cancer to Neurodegenerative Disorders

Missiroli

Genovese

Perrone

et al. 2020

JCM

171

124

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The main features that are commonly attributed to mitochondria consist of the regulation of cell proliferation, ATP generation, cell death and metabolism. However, recent scientific advances reveal that the intrinsic dynamicity of the mitochondrial compartment also plays a central role in proinflammatory signaling, identifying these organelles as a central platform for the control of innate immunity and the inflammatory response. Thus, mitochondrial dysfunctions have been related to severe chronic inflammatory disorders. Strategies aimed at reestablishing normal mitochondrial physiology could represent both preventive and therapeutic interventions for various pathologies related to exacerbated inflammation. Here, we explore the current understanding of the intricate interplay between mitochondria and the innate immune response in specific inflammatory diseases, such as neurological disorders and cancer.

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Section: Role Of Mitochondria and Neuroinflammation In Neurodegeneratmentioning

confidence: 99%

Section: Role Of Mitochondria and Neuroinflammation In Neurodegeneratmentioning

confidence: 99%

The Role of Mitochondria in Inflammation: From Cancer to Neurodegenerative Disorders

Missiroli

Genovese

Perrone

et al. 2020

JCM

171

124

View full text Add to dashboard Cite

show abstract

“…[ 129 ] Cuprizone‐induced demyelination models white matter abnormality in SCZ. [ 130 ] NAC could reverse the cognitive deficits and neurochemical deficits in the Cuprizone‐induced SCZ mouse model. [ 131 ] Txnrd2 knockdown results in deficits of mitochondrial integrity, cortical connectivity, and cognitive behavior, which were restored by NAC.…”

Section: Mitochondrial Function As a Potential Therapeutic Target Formentioning

confidence: 99%

Mitochondrial Dysfunction in Schizophrenia

Chung

2020

BioEssays

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Schizophrenia (SCZ) is a severe neurodevelopmental disorder affecting 1% of populations worldwide with a grave disability and socioeconomic burden. Current antipsychotic medications are effective treatments for positive symptoms, but poorly address negative symptoms and cognitive symptoms, warranting the development of better treatment options. Further understanding of SCZ pathogenesis is critical in these endeavors. Accumulating evidence has pointed to the role of mitochondria and metabolic dysregulation in SCZ pathogenesis. This review critically summarizes recent studies associating a compromised mitochondrial function with people with SCZ, including postmortem studies, imaging studies, genetic studies, and induced pluripotent stem cell studies. This review also discusses animal models with mitochondrial dysfunction resulting in SCZ-relevant neurobehavioral abnormalities, as well as restoration of mitochondrial function as potential therapeutic targets. Further understanding of mitochondrial dysfunction in SCZ may open the door to develop novel therapeutic strategies that can address the symptoms that cannot be adequately addressed by current antipsychotics alone.

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“…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.…”

Section: Introductionmentioning

confidence: 99%