Mast cells and neuroinflammation in pathogenesis of neurologic and psychiatric diseases

2021 ◽  
Vol 21 (2) ◽  
pp. 7-24
Author(s):  
Igor P. Grigorev ◽  
Dmitrii E. Korzhevskii

The review summarizes current data on the role of neuroinflammation and mast cells in the pathogenesis of nervous and mental diseases, such as multiple sclerosis, Alzheimers disease, Parkinsons disease, amyotrophic lateral sclerosis, depression, autism, migraine, schizophrenia and some others. The contribution of neuroinflammation to the pathogenesis of many of these diseases has been demonstrated. The involvement of mast cells in the development of the neuroinflammatory process has with varying degrees of evidence been shown for multiple sclerosis, amyotrophic lateral sclerosis, Alzheimers disease and migraine. There is still no convincing evidence that mast cells contribute to neuroinflammation in Parkinsons disease, depression, schizophrenia and autism spectrum disorder, although it is possible that they play a role in the pathogenesis of these diseases. Data on the causal role of neuroinflammation and mast cells in the development of neuropsychiatric diseases may become the basis for the development of new approaches to their pharmacological treatment. The review provides data on the first clinical trials of anti-inflammatory and mast cell activity-modulating drugs for the treatment of migraine, Alzheimers disease, multiple sclerosis and amyotrophic lateral sclerosis.

Biomolecules ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 1017
Author(s):  
Chiara Porro ◽  
Antonia Cianciulli ◽  
Maria Antonietta Panaro

IL-10, an immunosuppressive cytokine, is considered an important anti-inflammatory modulator of glial activation, preventing inflammation-mediated neuronal degeneration under pathological conditions. In this narrative review, we summarize recent insights about the role of IL-10 in the neurodegeneration associated with neuroinflammation, in diseases such as Multiple Sclerosis, Traumatic Brain Injury, Amyotrophic lateral sclerosis, Alzheimer’s Disease, and Parkinson’s Disease, focusing on the contribution of this cytokine not only in terms of protective action, but also as possibly responsible for clinical worsening. The knowledge of this double face of the same coin, regarding the biological role of the IL-10, could aid the development of targeted therapies useful for limiting neurodegenerative processes.


2012 ◽  
Vol 119 (2) ◽  
pp. 225-234 ◽  
Author(s):  
Judit Füvesi ◽  
Cecilia Rajda ◽  
Krisztina Bencsik ◽  
József Toldi ◽  
László Vécsei

2010 ◽  
Vol 9 (3) ◽  
pp. 268-278 ◽  
Author(s):  
Livia Pasquali ◽  
Riccardo Ruffoli ◽  
Federica Fulceri ◽  
Sara Pietracupa ◽  
Gabriele Siciliano ◽  
...  

2021 ◽  
pp. 1-15
Author(s):  
Vasily Vorobyov ◽  
Alexander Deev ◽  
Frank Sengpiel ◽  
Vladimir Nebogatikov ◽  
Aleksey A. Ustyugov

Background: Amyotrophic lateral sclerosis (ALS) is characterized by degeneration of motor neurons resulting in muscle atrophy. In contrast to the lower motor neurons, the role of upper (cortical) neurons in ALS is yet unclear. Maturation of locomotor networks is supported by dopaminergic (DA) projections from substantia nigra to the spinal cord and striatum. Objective: To examine the contribution of DA mediation in the striatum-cortex networks in ALS progression. Methods: We studied electroencephalogram (EEG) from striatal putamen (Pt) and primary motor cortex (M1) in ΔFUS(1–359)-transgenic (Tg) mice, a model of ALS. EEG from M1 and Pt were recorded in freely moving young (2-month-old) and older (5-month-old) Tg and non-transgenic (nTg) mice. EEG spectra were analyzed for 30 min before and for 60 min after systemic injection of a DA mimetic, apomorphine (APO), and saline. Results: In young Tg versus nTg mice, baseline EEG spectra in M1 were comparable, whereas in Pt, beta activity in Tg mice was enhanced. In older Tg versus nTg mice, beta dominated in EEG from both M1 and Pt, whereas theta and delta 2 activities were reduced. In younger Tg versus nTg mice, APO increased theta and decreased beta 2 predominantly in M1. In older mice, APO effects in these frequency bands were inversed and accompanied by enhanced delta 2 and attenuated alpha in Tg versus nTg mice. Conclusion: We suggest that revealed EEG modifications in ΔFUS(1–359)-transgenic mice are associated with early alterations in the striatum-cortex interrelations and DA transmission followed by adaptive intracerebral transformations.


Author(s):  
Luis De-Bernardi-Ojuel ◽  
Laura Torres-Collado ◽  
Manuela García-de-la-Hera

This scoping review aims to describe occupational therapy interventions carried out with multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS) patients in occupational therapy. A peer review of the literature was conducted in different databases: Pubmed, Scopus, Web of Science and Embase, and in some occupational therapy journals. A search of the literature published was carried out before December 2019. The inclusion criteria were as follows: (1) articles evaluating the intervention of occupational therapy in MS or ALS including experimental, randomized, nonrandomized and exploratory studies; (2) written in English or Spanish; (3) adult population (over 18 years old). The initial search identified 836 articles of which we included 32 divided into four areas of intervention: fatigue-targeted interventions, cognitive interventions, physical interventions and others. Only 16 studies were carried out exclusively by occupational therapists. Most occupational therapy interventions are aimed at fatigue and physical rehabilitation. The majority of the studies in our review included MS patients, with little representation from the ALS population. These interventions have shown an improvement in perceived fatigue, manual dexterity, falls prevention and improvement in cognitive aspects such as memory, communication, depression and quality of life in the MS and ALS populations.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Carmen N. Hernández-Candia ◽  
Sarah Pearce ◽  
Chandra L. Tucker

AbstractDynamic membraneless compartments formed by protein condensates have multifunctional roles in cellular biology. Tools that inducibly trigger condensate formation have been useful for exploring their cellular function, however, there are few tools that provide inducible control over condensate disruption. To address this need we developed DisCo (Disassembly of Condensates), which relies on the use of chemical dimerizers to inducibly recruit a ligand to the condensate-forming protein, triggering condensate dissociation. We demonstrate use of DisCo to disrupt condensates of FUS, associated with amyotrophic lateral sclerosis, and to prevent formation of polyglutamine-containing huntingtin condensates, associated with Huntington’s disease. In addition, we combined DisCo with a tool to induce condensates with light, CRY2olig, achieving bidirectional control of condensate formation and disassembly using orthogonal inputs of light and rapamycin. Our results demonstrate a method to manipulate condensate states that will have broad utility, enabling better understanding of the biological role of condensates in health and disease.


Antioxidants ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 11
Author(s):  
Cadiele Oliana Reichert ◽  
Debora Levy ◽  
Sergio P. Bydlowski

The human body has biological redox systems capable of preventing or mitigating the damage caused by increased oxidative stress throughout life. One of them are the paraoxonase (PON) enzymes. The PONs genetic cluster is made up of three members (PON1, PON2, PON3) that share a structural homology, located adjacent to chromosome seven. The most studied enzyme is PON1, which is associated with high density lipoprotein (HDL), having paraoxonase, arylesterase and lactonase activities. Due to these characteristics, the enzyme PON1 has been associated with the development of neurodegenerative diseases. Here we update the knowledge about the association of PON enzymes and their polymorphisms and the development of multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Parkinson’s disease (PD).


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