The Role of Gut Microbiota and Gut–Brain Interplay in Selected Diseases of the Central Nervous System DOI Open Access
Julia Doroszkiewicz, Magdalena Groblewska, Barbara Mroczko

et al.

International Journal of Molecular Sciences, Journal Year: 2021, Volume and Issue: 22(18), P. 10028 - 10028

Published: Sept. 17, 2021

The gut microbiome has attracted increasing attention from researchers in recent years. microbiota can have a specific and complex cross-talk with the host, particularly central nervous system (CNS), creating so-called “gut–brain axis”. Communication between gut, intestinal microbiota, brain involves secretion of various metabolites such as short-chain fatty acids (SCFAs), structural components bacteria, signaling molecules. Moreover, an imbalance composition modulates immune function tissue barriers blood–brain barrier (BBB). Therefore, aim this literature review is to describe how gut–brain interplay may contribute development neurological disorders, combining fields gastroenterology neuroscience. We present findings concerning effect altered on neurodegeneration neuroinflammation, including Alzheimer’s Parkinson’s diseases, well multiple sclerosis. impact pathological shift selected neuropsychological i.e., major depressive disorders (MDD) autism spectrum disorder (ASD), also discussed. Future research balanced axis would help identify new potential opportunities for therapeutic interventions presented diseases.

Language: Английский

Role of neuroinflammation in neurodegeneration development DOI Creative Commons
Weifeng Zhang, Dan Xiao, Qinwen Mao

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2023, Volume and Issue: 8(1)

Published: July 12, 2023

Abstract Studies in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and Amyotrophic lateral sclerosis, Huntington’s so on, have suggested that inflammation is not only a result of neurodegeneration but also crucial player this process. Protein aggregates which are very common pathological phenomenon can induce neuroinflammation further aggravates protein aggregation neurodegeneration. Actually, even happens earlier than aggregation. Neuroinflammation induced by genetic variations CNS cells or peripheral immune may deposition some susceptible population. Numerous signaling pathways range been to be involved the pathogenesis neurodegeneration, although they still far from being completely understood. Due limited success traditional treatment methods, blocking enhancing inflammatory considered promising strategies for therapy many them got exciting results animal models clinical trials. Some them, few, approved FDA usage. Here we comprehensively review factors affecting major pathogenicity sclerosis. We summarize current strategies, both clinic, diseases.

Language: Английский

Citations

555

GLP-1 Receptor Agonists: Beyond Their Pancreatic Effects DOI Creative Commons
Xin Zhao, Minghe Wang,

Zhitong Wen

et al.

Frontiers in Endocrinology, Journal Year: 2021, Volume and Issue: 12

Published: Aug. 23, 2021

Glucagon like peptide-1 (GLP-1) is an incretin secretory molecule. GLP-1 receptor agonists (GLP-1RAs) are widely used in the treatment of type 2 diabetes (T2DM) due to their attributes such as body weight loss, protection islet β cells, promotion cell proliferation and minimal side effects. Studies have found that GLP-1R distributed on pancreatic other tissues has multiple biological effects, reducing neuroinflammation, promoting nerve growth, improving heart function, suppressing appetite, delaying gastric emptying, regulating blood lipid metabolism fat deposition. Moreover, GLP-1RAs neuroprotective, anti-infectious, cardiovascular protective, metabolic regulatory exhibiting good application prospects. Growing attention been paid relationship between tumorigenesis, development prognosis patient with T2DM. Here, we reviewed therapeutic effects possible mechanisms action nervous, cardiovascular, endocrine systems correlation metabolism, tumours diseases.

Language: Английский

Citations

253

Clinical application of mesenchymal stem cell in regenerative medicine: a narrative review DOI Creative Commons
Ria Margiana, Alexander Markov, Angelina Olegovna Zekiy

et al.

Stem Cell Research & Therapy, Journal Year: 2022, Volume and Issue: 13(1)

Published: July 28, 2022

Abstract The multipotency property of mesenchymal stem cells (MSCs) has attained worldwide consideration because their immense potential for immunomodulation and therapeutic function in tissue regeneration. MSCs can migrate to injury areas contribute immune modulation, secrete anti-inflammatory cytokines hide themselves from the system. Certainly, various investigations have revealed anti-inflammatory, anti-aging, reconstruction, wound healing potentials many vitro vivo models. Moreover, current progresses field biology facilitated progress particular guidelines quality control approaches, which eventually lead clinical application MSCs. In this literature, we provided a brief overview immunoregulatory characteristics immunosuppressive activities addition, discussed enhancement, utilization, responses neural, liver, kidney, bone, heart diseases, healing.

Language: Английский

Citations

230

Neuroprotective effects of flavone luteolin in neuroinflammation and neurotrauma DOI
Duraisamy Kempuraj, Ramasamy Thangavel,

Deepak D. Kempuraj

et al.

BioFactors, Journal Year: 2020, Volume and Issue: 47(2), P. 190 - 197

Published: Oct. 24, 2020

Abstract Neuroinflammation leads to neurodegeneration, cognitive defects, and neurodegenerative disorders. Neurotrauma/traumatic brain injury (TBI) can cause activation of glial cells, neurons, neuroimmune cells in the release neuroinflammatory mediators. Neurotrauma immediate primary damage (direct damage), responses, neuroinflammation, late secondary (indirect) through mechanism. Secondary chronic inflammation onset progression diseases. Currently, there are no effective specific therapeutic options treat these damages or Flavone luteolin is an important natural polyphenol present several plants that show anti‐inflammatory, antioxidant, anticancer, cytoprotective, macrophage polarization effects. In this short review article, we have reviewed neuroprotective effects neurotrauma disorders pathways involved We collected data for study from publications PubMed using keywords mast diseases, TBI. Recent reports suggest suppresses systemic responses Coronavirus disease 2019 (COVID‐19). Studies shown exhibits various mechanisms, including suppressing immune cell activation, such as inflammatory mediators released cells. addition, suppress response, microglia astrocytes, oxidative stress, severity diseases Alzheimer's disease, Parkinson's multiple sclerosis, TBI pathogenesis. conclusion, improve decline enhance neuroprotection TBI, stroke.

Language: Английский

Citations

166

A Historical Review of Brain Drug Delivery DOI Creative Commons
William M. Pardridge

Pharmaceutics, Journal Year: 2022, Volume and Issue: 14(6), P. 1283 - 1283

Published: June 16, 2022

The history of brain drug delivery is reviewed beginning with the first demonstration, in 1914, that a for syphilis, salvarsan, did not enter brain, due to presence blood–brain barrier (BBB). Owing restricted transport across BBB, FDA-approved drugs CNS have been generally limited lipid-soluble small molecules. Drugs do cross BBB can be re-engineered on endogenous carrier-mediated and receptor-mediated systems, which were identified during 1970s–1980s. By 1990s, multitude technologies emerged, including trans-cranial delivery, CSF disruption, lipid carriers, prodrugs, stem cells, exosomes, nanoparticles, gene therapy, biologics. advantages limitations each these are critically reviewed.

Language: Английский

Citations

137

A Perspective on Nrf2 Signaling Pathway for Neuroinflammation: A Potential Therapeutic Target in Alzheimer's and Parkinson's Diseases DOI Creative Commons
Sarmistha Saha, Brigitta Buttari, Elisabetta Profumo

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2022, Volume and Issue: 15

Published: Jan. 21, 2022

Neuroinflammation plays a pivotal role in Alzheimer's disease (AD) and Parkinson's (PD), the leading causes of dementia. These neurological disorders are characterized by accumulation misfolded proteins such as amyloid-ß (Aß), tau protein α-synuclein, contributing to mitochondrial fragmentation, oxidative stress, neuroinflammation. Misfolded activate microglia, which induces neuroinflammation, expression pro-inflammatory cytokines subsequently facilitates synaptic damage neuronal loss. So far, all proposed drugs were based on inhibition aggregation failed clinical trials. Therefore, treatment options dementia still challenging issue. Thus, it is worthwhile study alternative therapeutic strategies. In this context, there increasing data transcription factor NF- E2 p45-related 2 (Nrf2) redox homeostasis anti-inflammatory functions neurodegenerative disorders. Interestingly, Nrf2 signaling pathway has shown upregulation antioxidant genes, microglia-mediated inflammation, improved function diseases, suggesting activation could be novel approach target pathogenesis. The present review will examine correlation between with neuroinflammation AD PD.

Language: Английский

Citations

132

From imbalance to impairment: the central role of reactive oxygen species in oxidative stress-induced disorders and therapeutic exploration DOI Creative Commons
Sheryar Afzal, Aimi Syamima Abdul Manap, Ali Attiq

et al.

Frontiers in Pharmacology, Journal Year: 2023, Volume and Issue: 14

Published: Oct. 18, 2023

Increased production and buildup of reactive oxygen species (ROS) can lead to various health issues, including metabolic problems, cancers, neurological conditions. Our bodies counteract ROS with biological antioxidants such as SOD, CAT, GPx, which help prevent cellular damage. However, if there is an imbalance between these antioxidants, it result in oxidative stress. This cause genetic epigenetic changes at the molecular level. review delves into how plays a role disorders caused by We also look animal models used for researching pathways. study offers insights mechanism, pathology, changes, assist drug development disease understanding.

Language: Английский

Citations

117

Targeting Microglial α-Synuclein/TLRs/NF-kappaB/NLRP3 Inflammasome Axis in Parkinson’s Disease DOI Creative Commons

Yunna Li,

Yun Xia,

Sijia Yin

et al.

Frontiers in Immunology, Journal Year: 2021, Volume and Issue: 12

Published: Oct. 8, 2021

According to emerging studies, the excessive activation of microglia and subsequent release pro-inflammatory cytokines play important roles in pathogenesis progression Parkinson’s disease (PD). However, exact mechanisms governing chronic neuroinflammation remain elusive. Findings demonstrate an elevated level NLRP3 inflammasome activated substantia nigra PD patients. Activated aggravates pathology accelerates neurodegenerative diseases. Abnormal protein aggregation α-synuclein (α-syn), a pathologically relevant PD, were reported activate through interaction with toll-like receptors (TLRs). This eventually releases translocation nuclear factor kappa-B (NF-κB) causes impairment mitochondria, thus damaging dopaminergic neurons. Currently, therapeutic drugs for are primarily aimed at providing relief from its clinical symptoms, there no well-established strategies halt or reverse this disease. In review, we update existing knowledge on role α-syn/TLRs/NF-κB/NLRP3 axis microglial PD. addition, review summarizes recent progress as potential target treatment by inhibiting activation.

Language: Английский

Citations

115

CX3CL1/CX3CR1 signaling targets for the treatment of neurodegenerative diseases DOI

Meena S. Subbarayan,

Aurélie Joly‐Amado,

Paula C. Bickford

et al.

Pharmacology & Therapeutics, Journal Year: 2021, Volume and Issue: 231, P. 107989 - 107989

Published: Sept. 4, 2021

Language: Английский

Citations

107

Epstein-Barr Virus and Neurological Diseases DOI Creative Commons
Nan Zhang,

Yuxin Zuo,

Liping Jiang

et al.

Frontiers in Molecular Biosciences, Journal Year: 2022, Volume and Issue: 8

Published: Jan. 10, 2022

Epstein-Barr virus (EBV), also known as human herpesvirus 4, is a double-stranded DNA that ubiquitous in 90-95% of the population gamma herpesvirus. It exists two main states, latent infection and lytic replication, each encoding viral proteins with different functions. Human B-lymphocytes epithelial cells are EBV-susceptible host cells. EBV latently infects B nasopharyngeal throughout life most immunologically active individuals. EBV-infected cells, free viruses, their gene products, abnormally elevated titers observed cerebrospinal fluid. Studies have shown can infect neurons directly or indirectly via infected B-lymphocytes, induce neuroinflammation demyelination, promote proliferation, degeneration, necrosis glial proliferative disorders B- T-lymphocytes, contribute to occurrence development nervous system diseases, such Alzheimer's disease, Parkinson's multiple sclerosis, acute cerebellar ataxia, meningitis, disseminated encephalomyelitis, brain tumors. However, specific underlying molecular mechanisms unclear. In this paper, we review role central which could bebeneficial providing new research ideas potential clinical therapeutic targets for neurological diseases.

Language: Английский

Citations

97