scholarly journals Neuroproteomics in Epilepsy: What Do We Know so Far?

2021 ◽  
Vol 13 ◽  
Author(s):  
Amanda M. do Canto ◽  
Amanda Donatti ◽  
Jaqueline C. Geraldis ◽  
Alexandre B. Godoi ◽  
Douglas C. da Rosa ◽  
...  
Keyword(s):  
Neurological Disorders ◽  
Neural Circuit ◽  
Neurological Diseases ◽  
Epileptic Seizures ◽  
World Population ◽  
Social Burden ◽  
Neuronal Excitation ◽  
System A ◽  
Underlying Mechanisms ◽  
Patients With Epilepsy

Epilepsies are chronic neurological diseases that affect approximately 2% of the world population. In addition to being one of the most frequent neurological disorders, treatment for patients with epilepsy remains a challenge, because a proportion of patients do not respond to the antiseizure medications that are currently available. This results in a severe economic and social burden for patients, families, and the healthcare system. A characteristic common to all forms of epilepsy is the occurrence of epileptic seizures that are caused by abnormal neuronal discharges, leading to a clinical manifestation that is dependent on the affected brain region. It is generally accepted that an imbalance between neuronal excitation and inhibition generates the synchronic electrical activity leading to seizures. However, it is still unclear how a normal neural circuit becomes susceptible to the generation of seizures or how epileptogenesis is induced. Herein, we review the results of recent proteomic studies applied to investigate the underlying mechanisms leading to epilepsies and how these findings may impact research and treatment for these disorders.

scholarly journals Microglial Cell Morphology and Phagocytic Activity Are Critically Regulated by the Neurosteroid Allopregnanolone: A Possible Role in Neuroprotection

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 698
Author(s):  
Valérie Jolivel ◽  
Susana Brun ◽  
Fabien Binamé ◽  
Jérémie Benyounes ◽  
Omar Taleb ◽  
...  
Keyword(s):  
Neurological Disorders ◽  
Phagocytic Activity ◽  
Microglial Cell ◽  
Neurological Diseases ◽  
Time Lapse ◽  
Microglial Cells ◽  
Primary Microglia ◽  
Gaba A ◽  
Neuroprotective Strategies ◽  
Underlying Mechanisms

Microglial cells are key players in neural pathogenesis and microglial function regulation appears to be pivotal in controlling neuroinflammatory/neurological diseases. Here, we investigated the effects and mechanism of action of neurosteroid allopregnanolone (ALLO) on murine microglial BV-2 cells and primary microglia in order to determine ALLO-induced immunomodulatory potential and to provide new insights for the development of both natural and safe neuroprotective strategies targeting microglia. Indeed, ALLO-treatment is increasingly suggested as beneficial in various models of neurological disorders but the underlying mechanisms have not been elucidated. Therefore, the microglial cells were cultured with various serum concentrations to mimic the blood-brain-barrier rupture and to induce their activation. Proliferation, viability, RT-qPCR, phagocytosis, and morphology analyzes, as well as migration with time-lapse imaging and quantitative morphodynamic methods, were combined to investigate ALLO actions on microglia. BV-2 cells express subunits of GABA-A receptor that mediates ALLO activity. ALLO (10µM) induced microglial cell process extension and decreased migratory capacity. Interestingly, ALLO modulated the phagocytic activity of BV-2 cells and primary microglia. Our results, which show a direct effect of ALLO on microglial morphology and phagocytic function, suggest that the natural neurosteroid-based approach may contribute to developing effective strategies against neurological disorders that are evoked by microglia-related abnormalities.

scholarly journals The effect of epilepsy control on psychogenic non epileptic seizures

2021 ◽  
Author(s):  
Muaz.A.Ibrahim ◽  
Tasneem.M.F ◽  
Khabab Abbasher Hussien Mohamed Ahmed ◽  
Abdallah M. Abdallah ◽  
Mohammed Eltahier Abdalla Omer ◽  
...  
Keyword(s):  
Epileptic Seizure ◽  
Focal Epilepsy ◽  
Neurological Diseases ◽  
Epileptic Seizures ◽  
Abnormal Behavior ◽  
Detailed History ◽  
Follow Up Care ◽  
History Of ◽  
Patients With Epilepsy

Abstract Background: Epilepsy is one of the most common neurological diseases. The coexistence of epilepsy and PNES poses a major challenge to neurologists and psychiatrists in the treatment and follow-up care of patients. Methods: 33 Sudanese patients with epilepsy and concomitant psychogenic non epileptic seizure where included in this study and full detailed history of both epilepsy and PNES was obtained. The study was conducted in Daoud charity clinic during the period from May to July 2018Results : Out of 33 patients 19 were males and 14 were females. Seven patients had focal epilepsy, 23 had generalized tonic clonic epilepsy (GTC), 2 had GTC with atypical absent seizure, and one had GTC with myoclonus.Six patients experienced an attack of PNES after more than 1 year of being free of epilepsy, while 9 patients had PNES attack between 3 months to 1 year of the last attack of epilepsy, and 18 patients developed both PNES and epilepsy within less than 3 months.The pattern of presentation of PNES was bizarre movements in 13 patients, abnormal behavior in 9 patients, while 11 patients experienced both bizarre movement and abnormal behavior note that all those 11 patients had GTC epilepsy. Conclusion: Experiencing psychogenic non epileptic seizure (PNES) in patients with coexisting PNES and epilepsy is not affected by the epilepsy free period

scholarly journals The Cross Talk between Underlying Mechanisms of Multiple Sclerosis and Epilepsy May Provide New Insights for More Efficient Therapies

2021 ◽  
Vol 14 (10) ◽  
pp. 1031
Author(s):  
Atefeh Rayatpour ◽  
Sahar Farhangi ◽  
Ester Verdaguer ◽  
Jordi Olloquequi ◽  
Jesus Ureña ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
General Population ◽  
Neurodegenerative Diseases ◽  
Cross Talk ◽  
Huntington Disease ◽  
Neurological Disorders ◽  
Epileptic Seizures ◽  
Bidirectional Association ◽  
The Common ◽  
Underlying Mechanisms

Despite the significant differences in pathological background of neurodegenerative diseases, epileptic seizures are a comorbidity in many disorders such as Huntington disease (HD), Alzheimer’s disease (AD), and multiple sclerosis (MS). Regarding the last one, specifically, it has been shown that the risk of developing epilepsy is three to six times higher in patients with MS compared to the general population. In this context, understanding the pathological processes underlying this connection will allow for the targeting of the common and shared pathological pathways involved in both conditions, which may provide a new avenue in the management of neurological disorders. This review provides an outlook of what is known so far about the bidirectional association between epilepsy and MS.

scholarly journals From Metabolic Syndrome to Neurological Diseases: Role of Autophagy

2021 ◽  
Vol 9 ◽  
Author(s):  
Jessica Maiuolo ◽  
Micaela Gliozzi ◽  
Vincenzo Musolino ◽  
Cristina Carresi ◽  
Federica Scarano ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Disease Risk ◽  
Neurological Diseases ◽  
Cardiovascular Disease Risk ◽  
Systemic Hypertension ◽  
Atherogenic Dyslipidemia ◽  
World Population ◽  
Intracellular Process ◽  
The Central Nervous System ◽  
Underlying Mechanisms

Metabolic syndrome is not a single pathology, but a constellation of cardiovascular disease risk factors including: central and abdominal obesity, systemic hypertension, insulin resistance (or type 2 diabetes mellitus), and atherogenic dyslipidemia. The global incidence of Metabolic syndrome is estimated to be about one quarter of the world population; for this reason, it would be desirable to better understand the underlying mechanisms involved in order to develop treatments that can reduce or eliminate the damage caused. The effects of Metabolic syndrome are multiple and wide ranging; some of which have an impact on the central nervous system and cause neurological and neurodegenerative diseases. Autophagy is a catabolic intracellular process, essential for the recycling of cytoplasmic materials and for the degradation of damaged cellular organelle. Therefore, autophagy is primarily a cytoprotective mechanism; even if excessive cellular degradation can be detrimental. To date, it is known that systemic autophagic insufficiency is able to cause metabolic balance deterioration and facilitate the onset of metabolic syndrome. This review aims to highlight the current state of knowledge regarding the connection between metabolic syndrome and the onset of several neurological diseases related to it. Furthermore, since autophagy has been found to be of particular importance in metabolic disorders, the probable involvement of this degradative process is assumed to be responsible for the attenuation of neurological disorders resulting from metabolic syndrome.

scholarly journals Neural circuit repair by low-intensity magnetic stimulation requires cellular magnetoreceptors and specific stimulation patterns

2019 ◽  
Vol 5 (10) ◽  
pp. eaav9847 ◽  
Author(s):  
T. Dufor ◽  
S. Grehl ◽  
A. D. Tang ◽  
M. Doulazmi ◽  
M. Traoré ◽  
...  
Keyword(s):  
Magnetic Stimulation ◽  
Neural Circuit ◽  
Ex Vivo ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Neurological Diseases ◽  
Low Intensity ◽  
Electromagnetic Stimulation ◽  
Weak Magnetic Fields ◽  
Underlying Mechanisms

Although electromagnetic brain stimulation is a promising treatment in neurology and psychiatry, clinical outcomes are variable, and underlying mechanisms are ill-defined, which impedes the development of new effective stimulation protocols. Here, we show, in vivo and ex vivo, that repetitive transcranial magnetic stimulation at low-intensity (LI-rTMS) induces axon outgrowth and synaptogenesis to repair a neural circuit. This repair depends on stimulation pattern, with complex biomimetic patterns being particularly effective, and the presence of cryptochrome, a putative magnetoreceptor. Only repair-promoting LI-rTMS patterns up-regulated genes involved in neuronal repair; almost 40% of were cryptochrome targets. Our data open a new framework to understand the mechanisms underlying structural neuroplasticity induced by electromagnetic stimulation. Rather than neuronal activation by induced electric currents, we propose that weak magnetic fields act through cryptochrome to activate cellular signaling cascades. This information opens new routes to optimize electromagnetic stimulation and develop effective treatments for different neurological diseases.

The use of progesterone during pregnancy in women with epilepsy as an alternative to the correction of doses of anticonvulsants

GYNECOLOGY ◽  
2020 ◽  
Vol 21 (6) ◽  
pp. 12-15
Author(s):  
Elena V. Tsallagova ◽  
Vasily O. Generalov ◽  
Timur R. Sadykov
Keyword(s):  
Clinical Remission ◽  
Epileptic Seizures ◽  
Progesterone Concentration ◽  
Teratogenic Effects ◽  
Safe Alternative ◽  
Patients With Epilepsy

Pregnancy is the most dangerous period in terms of interruption of even persistent and long-term remission. At the same time increasing the dose of anticonvulsant increases the risk of teratogenic effects. Aim. to assess the possibility of using progesterone to prevent relapse of epileptic seizures during pregnancy. Materials and methods. 38 pregnant patients with epilepsy with clinical remission before pregnancy, with relapse of epileptic seizures in I trimester of pregnancy, age 31.81.4 years. Dydrogesterone in a dose of 10 to 60 mg/day was prescribed after the relapse of remission. Anticonvulsant dosage was not changed. The blood progesterone concentration and EEG control was carried out. Results. During pregnancy, the level of progesterone in the blood gradually increased from 77.8 nmol/l at 78 weeks of pregnancy to 521.1 nmol/l at 3637 weeks of pregnancy, without exceeding the limits. EEG results did not deteriorate. None of the patients had seizures during pregnancy. Conclusion. Progesterone therapy is an adequate and safe alternative to increasing the dose of anticonvulsants in case of recurrent seizures during pregnancy.

Mills' syndrome. A clinical case of a rare degenerative pathology of the central nervous system

2020 ◽  
pp. 57-60
Author(s):  
Konstantin Gulyabin
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurological Diseases ◽  
Cortical Atrophy ◽  
Primary Lateral Sclerosis ◽  
System A ◽  
The Central Nervous System ◽  
Primary Lateral ◽  
Lateral Sclerosis ◽  
Mills Syndrome

Mills' syndrome is a rare neurological disorder. Its nosological nature is currently not completely determined. Nevertheless, Mills' syndrome is considered to be a rare variant of the degenerative pathology of the central nervous system – a variant of focal cortical atrophy. The true prevalence of this pathology is unknown, since this condition is more often of a syndrome type, observed in the clinical picture of a number of neurological diseases (primary lateral sclerosis, frontotemporal dementia, etc.) and is less common in isolated form.

Autophagy Modulators and Neuroinflammation

2020 ◽  
Vol 27 (6) ◽  
pp. 955-982 ◽  
Author(s):  
Kyoung Sang Cho ◽  
Jang Ho Lee ◽  
Jeiwon Cho ◽  
Guang-Ho Cha ◽  
Gyun Jee Song
Keyword(s):  
Neurodegenerative Disorders ◽  
Neurological Disorders ◽  
Mammalian Cells ◽  
Critical Role ◽  
Therapeutic Agents ◽  
Mechanisms Of Action ◽  
Scientific Interest ◽  
Therapeutic Tools ◽  
Underlying Mechanisms

Background: Neuroinflammation plays a critical role in the development and progression of various neurological disorders. Therefore, various studies have focused on the development of neuroinflammation inhibitors as potential therapeutic tools. Recently, the involvement of autophagy in the regulation of neuroinflammation has drawn substantial scientific interest, and a growing number of studies support the role of impaired autophagy in the pathogenesis of common neurodegenerative disorders. Objective: The purpose of this article is to review recent research on the role of autophagy in controlling neuroinflammation. We focus on studies employing both mammalian cells and animal models to evaluate the ability of different autophagic modulators to regulate neuroinflammation. Methods: We have mostly reviewed recent studies reporting anti-neuroinflammatory properties of autophagy. We also briefly discussed a few studies showing that autophagy modulators activate neuroinflammation in certain conditions. Results: Recent studies report neuroprotective as well as anti-neuroinflammatory effects of autophagic modulators. We discuss the possible underlying mechanisms of action of these drugs and their potential limitations as therapeutic agents against neurological disorders. Conclusion: Autophagy activators are promising compounds for the treatment of neurological disorders involving neuroinflammation.

Microbiota-Immune System Interactions in Human Neurological Disorders

2020 ◽  
Vol 19 (7) ◽  
pp. 509-526
Author(s):  
Qin Huang ◽  
Fang Yu ◽  
Di Liao ◽  
Jian Xia
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Neurological Disorders ◽  
Brain Function ◽  
Neurological Diseases ◽  
Host Immune System ◽  
Gut Dysbiosis ◽  
Characteristic Features ◽  
Novel Therapeutic Strategies

: Recent studies implicate microbiota-brain communication as an essential factor for physiology and pathophysiology in brain function and neurodevelopment. One of the pivotal mechanisms about gut to brain communication is through the regulation and interaction of gut microbiota on the host immune system. In this review, we will discuss the role of microbiota-immune systeminteractions in human neurological disorders. The characteristic features in the development of neurological diseases include gut dysbiosis, the disturbed intestinal/Blood-Brain Barrier (BBB) permeability, the activated inflammatory response, and the changed microbial metabolites. Neurological disorders contribute to gut dysbiosis and some relevant metabolites in a top-down way. In turn, the activated immune system induced by the change of gut microbiota may deteriorate the development of neurological diseases through the disturbed gut/BBB barrier in a down-top way. Understanding the characterization and identification of microbiome-immune- brain signaling pathways will help us to yield novel therapeutic strategies by targeting the gut microbiome in neurological disease.

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