Electroconvulsive stimulation attenuates chronic neuroinflammation

Study background: Chronic neuroinflammation is a common emerging hallmark of several neurodegenerative diseases. Alzheimer’s Disease (AD) is the most common cause of dementia among the elderly and is characterized by loss of memory and other cognitive functions.

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Trombodynamics Method in the Assessment of Coagulation Parameters in Psychopharmacotherapy of Endogenous Mental Disorders

Psychiatry ◽

10.30629/2618-6667-2020-18-4-16-25 ◽

2020 ◽

Vol 18 (4) ◽

pp. 16-25

Author(s):

N. S. Karpova ◽

O. S. Brusov ◽

I. V. Oleichik ◽

M. I. Faktor ◽

N. S. Levchenko ◽

...

Keyword(s):

Mental Disorders ◽

Response To Therapy ◽

Procoagulant Activity ◽

Coagulation Activity ◽

Continuous Type ◽

Chronic Neuroinflammation ◽

Psychopharmacological Treatment ◽

Before And After ◽

First Time ◽

Schizotypal Disorder

Background: currently, it has been proven that the pathogenesis of endogenous mental disorders is associated with the process of neuroinflammation in the brain of patients. It is also known that chronic neuroinflammation, accompanied by a violation the permeability of the blood-brain barrier. It is accompanied by the activation of platelets that generate procoagulant microparticles, which leads to a disturbance of the hemostasis system, causing an increase in blood clotting in patients. Objective: to investigate the dynamics of procoagulant activity of blood in patients with endogenous mental disorders before and after psychopharmacotherapy.Patients and methods: the study included 185 patients aged 16 to 64 years with the following mental disorders: schizophrenia with attack-like/attack-progressive/continuous type of course (F20.00–2), affective disease (F31.1–5; F32.0–3; F33.0–3), schizotypal disorder with affective fluctuations (F21.3–4). The thrombodynamic test (TD) was performed on T-2 Trombodynamis device according to the manufacturer’s instructions (Hemacore LLC, Moscow, Russia). All patients received standard pharmacotherapy according to their condition.Results: a significant decrease of procoagulant activity of spontaneous clots in the patients’ blood after psychopharmacological treatment is observed. Our data on the positive dynamics of changes in the values of TD test’s indicators in most of the examined patients suggest that a decrease in the coagulation activity of the patients’ blood as a result of treatment may be associated with the anti- inflammatory effect of antipsychotics and antidepressants.Conclusion: for the first time, it was shown that there is a positive dynamic in changing the values of the main parameters of the TD test in most patients with endogenous mental diseases. The results of TD tests can be the basis for monitoring the response to therapy.

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Sustained hippocampal IL-1β overexpression mediates chronic neuroinflammation and ameliorates Alzheimer plaque pathology

Journal of Clinical Investigation ◽

10.1172/jci31450 ◽

2007 ◽

Vol 117 (6) ◽

pp. 1595-1604 ◽

Cited By ~ 243

Author(s):

Solomon S. Shaftel ◽

Stephanos Kyrkanides ◽

John A. Olschowka ◽

Jen-nie H. Miller ◽

Renee E. Johnson ◽

...

Keyword(s):

Chronic Neuroinflammation ◽

Plaque Pathology

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The Potential Neuroprotective Role of Free and Encapsulated Quercetin Mediated by miRNA against Neurological Diseases

Nutrients ◽

10.3390/nu13041318 ◽

2021 ◽

Vol 13 (4) ◽

pp. 1318

Author(s):

Tarek Benameur ◽

Raffaella Soleti ◽

Chiara Porro

Keyword(s):

Inflammatory Responses ◽

Pathological Condition ◽

Neurological Diseases ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

In Vivo Studies ◽

Innovative Drug ◽

Chronic Neuroinflammation

Chronic neuroinflammation is a pathological condition of numerous central nervous system (CNS) diseases such as Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, amyotrophic lateral sclerosis and many others. Neuroinflammation is characterized by the microglia activation and concomitant production of pro-inflammatory cytokines leading to an increasing neuronal cell death. The decreased neuroinflammation could be obtained by using natural compounds, including flavonoids known to modulate the inflammatory responses. Among flavonoids, quercetin possess multiple pharmacological applications including anti-inflammatory, antitumoral, antiapoptotic and anti-thrombotic activities, widely demonstrated in both in vitro and in vivo studies. In this review, we describe the recent findings about the neuroprotective action of quercetin by acting with different mechanisms on the microglial cells of CNS. The ability of quercetin to influence microRNA expression represents an interesting skill in the regulation of inflammation, differentiation, proliferation, apoptosis and immune responses. Moreover, in order to enhance quercetin bioavailability and capacity to target the brain, we discuss an innovative drug delivery system. In summary, this review highlighted an important application of quercetin in the modulation of neuroinflammation and prevention of neurological disorders.

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α-Synuclein, a chemoattractant, directs microglial migration via H2O2-dependent Lyn phosphorylation

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1417883112 ◽

2015 ◽

Vol 112 (15) ◽

pp. E1926-E1935 ◽

Cited By ~ 69

Author(s):

Shijun Wang ◽

Chun-Hsien Chu ◽

Tessandra Stewart ◽

Carmen Ginghina ◽

Yifei Wang ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Cell Migration ◽

Neuronal Damage ◽

Directional Migration ◽

Chronic Neuroinflammation ◽

Tyrosine Protein Kinase ◽

Microglial Migration ◽

Directional Cell Migration ◽

Cytoskeleton Rearrangement

Malformed α-Synuclein (α-syn) aggregates in neurons are released into the extracellular space, activating microglia to induce chronic neuroinflammation that further enhances neuronal damage in α-synucleinopathies, such as Parkinson’s disease. The mechanisms by which α-syn aggregates activate and recruit microglia remain unclear, however. Here we show that α-syn aggregates act as chemoattractants to direct microglia toward damaged neurons. In addition, we describe a mechanism underlying this directional migration of microglia. Specifically, chemotaxis occurs when α-syn binds to integrin CD11b, leading to H2O2 production by NADPH oxidase. H2O2 directly attracts microglia via a process in which extracellularly generated H2O2 diffuses into the cytoplasm and tyrosine protein kinase Lyn, phosphorylates the F-actin–associated protein cortactin after sensing changes in the microglial intracellular concentration of H2O2. Finally, phosphorylated cortactin mediates actin cytoskeleton rearrangement and facilitates directional cell migration. These findings have significant implications, given that α-syn–mediated microglial migration reaches beyond Parkinson’s disease.

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Eomes-expressing T-helper cells as potential target of therapy in chronic neuroinflammation

Neurochemistry International ◽

10.1016/j.neuint.2018.11.023 ◽

2019 ◽

Vol 130 ◽

pp. 104348 ◽

Cited By ~ 2

Author(s):

Shinji Oki

Keyword(s):

T Helper Cells ◽

T Helper ◽

Potential Target ◽

Helper Cells ◽

Chronic Neuroinflammation

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Cromolyn Platform Suppresses Fibrosis and Inflammation, Promotes Microglial Phagocytosis and Neurite Outgrowth

10.21203/rs.3.rs-825684/v1 ◽

2021 ◽

Author(s):

Yi-Jun Wang ◽

Matthew A. Downey ◽

Sungwoon Choi ◽

Timothy M. Shoup ◽

David R. Elmaleh

Keyword(s):

Neurite Outgrowth ◽

Subsequent Treatment ◽

Human Microglia ◽

Microglial Phagocytosis ◽

Chronic Neuroinflammation ◽

Collagen Xviii ◽

Nerve Growth Factor Treatment ◽

The Central Nervous System ◽

Gsk 3Β ◽

Related Proteins

Abstract Neurodegenerative diseases are characterized by chronic neuroinflammation and may perpetuate ongoing fibrotic reactions within the central nervous system. In this report, RNA-seq analysis shows that administration of the pro-inflammatory cytokine TNF-α to HMC3 human microglia results in a robust upregulation of fibrosis-associated genes. Subsequent treatment with cromolyn and its fluorinated analogue F-cromolyn resulted in reduced secretion of collagen XVIII, fibronectin, and tenascin-c. Additionally, we show that cromolyn and F-cromolyn reduce secretion of pro-inflammatory proteins PLP1, PELP1, HSP90, IL-2, GRO-α, Eotaxin, and VEGF-Α, while promoting secretion of anti-inflammatory IL-4 in HMC3 microglia. Neurite outgrowth in PC12 neuronal cells is augmented by cromolyn and F-cromolyn in concert with nerve growth factor. Treatment also differentially altered secretion of neurogenesis-related proteins TTL, PROX1, Rab35, and CSDE1 in HMC3 microglia. Finally, iPSC-derived human microglia more readily phagocytose Aβ42 with cromolyn and F-cromolyn relative to controls. We propose the cromolyn platform targets multiple proteins upstream of PI3K/Akt/mTOR, NF-κB, and GSK-3β signaling pathways to affect cytokine, chemokine, and fibrosis-related protein expression.

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