RNA-binding proteins as a common ground for neurodegeneration and inflammation in amyotrophic lateral sclerosis and multiple sclerosis

Acosta-Galeana, Isabel; Hernández-Martínez, Ricardo; Reyes-Cruz, Tania; Chiquete, Erwin; Buendía, José de Jesús Aceves

doi:10.3389/fnmol.2023.1193636

Cited by 4 publications

(2 citation statements)

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“…Recently, immune dysregulation has been suspected [ 171 , 172 , 173 ], with neuroinflammation being invoked in general [ 174 , 175 , 176 ] and for ALS in particular [ 177 , 178 , 179 ], especially concerning activation of microglia and astrocytes [ 180 , 181 ]. It is interesting that microglia communicate with [ 182 ], and can be activated by [ 183 ], mast cells, unique effector immune cells that are ubiquitous in the body and are critical in allergies [ 184 ], but also inflammatory processes [ 185 ].…”

Section: Amyotrophic Lateral Sclerosis (Als)mentioning

confidence: 99%

Recent Research Trends in Neuroinflammatory and Neurodegenerative Disorders

Cohen,

Mathew,

Dourvetakis

et al. 2024

Cells

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Neuroinflammatory and neurodegenerative disorders including Alzheimer’s disease (AD), Parkinson’s disease (PD), traumatic brain injury (TBI) and Amyotrophic lateral sclerosis (ALS) are chronic major health disorders. The exact mechanism of the neuroimmune dysfunctions of these disease pathogeneses is currently not clearly understood. These disorders show dysregulated neuroimmune and inflammatory responses, including activation of neurons, glial cells, and neurovascular unit damage associated with excessive release of proinflammatory cytokines, chemokines, neurotoxic mediators, and infiltration of peripheral immune cells into the brain, as well as entry of inflammatory mediators through damaged neurovascular endothelial cells, blood–brain barrier and tight junction proteins. Activation of glial cells and immune cells leads to the release of many inflammatory and neurotoxic molecules that cause neuroinflammation and neurodegeneration. Gulf War Illness (GWI) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are chronic disorders that are also associated with neuroimmune dysfunctions. Currently, there are no effective disease-modifying therapeutic options available for these diseases. Human induced pluripotent stem cell (iPSC)-derived neurons, astrocytes, microglia, endothelial cells and pericytes are currently used for many disease models for drug discovery. This review highlights certain recent trends in neuroinflammatory responses and iPSC-derived brain cell applications in neuroinflammatory disorders.

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Section: Amyotrophic Lateral Sclerosis (Als)mentioning

confidence: 99%

Recent Research Trends in Neuroinflammatory and Neurodegenerative Disorders

Cohen,

Mathew,

Dourvetakis

et al. 2024

Cells

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“…Therefore, reactive microglia and astrocytes promote the release of immune mediators, including proinflammatory cytokines and chemokines; decrease the production of protective factors (growth factors, fractalkine, etc); and promote glutamate toxicity, all of which can promote the onset and progression of NDDs and thus represent potential therapeutic targets [68,69]. Notably, progressive MS is marked by similar activation of microglia [70,71].…”

Section: Overlapping Immune Imbalancementioning

confidence: 99%

Overlapping Neuroimmune Mechanisms and Therapeutic Targets in Neurodegenerative Disorders

De Marchi,

Munitic,

Vidatic

et al. 2023

Biomedicines

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Many potential immune therapeutic targets are similarly affected in adult-onset neurodegenerative diseases, such as Alzheimer’s (AD) disease, Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and frontotemporal dementia (FTD), as well as in a seemingly distinct Niemann–Pick type C disease with primarily juvenile onset. This strongly argues for an overlap in pathogenic mechanisms. The commonly researched immune targets include various immune cell subsets, such as microglia, peripheral macrophages, and regulatory T cells (Tregs); the complement system; and other soluble factors. In this review, we compare these neurodegenerative diseases from a clinical point of view and highlight common pathways and mechanisms of protein aggregation, neurodegeneration, and/or neuroinflammation that could potentially lead to shared treatment strategies for overlapping immune dysfunctions in these diseases. These approaches include but are not limited to immunisation, complement cascade blockade, microbiome regulation, inhibition of signal transduction, Treg boosting, and stem cell transplantation.

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