Physical Activity Regulates and Mediates the Signaling Pathway and Pathophysiological Mechanisms of the Neuroinflammation and Neurodegenerative DOI Open Access
Navid Abedpoor, Fatemeh Hajibabaie

Asian Journal of Sports Medicine, Journal Year: 2024, Volume and Issue: 15(4)

Published: Oct. 23, 2024

Context: The correlation between neuroinflammation and neurodegenerative disorders has been extensively documented. Elevated levels of inflammatory cytokines in the bloodstream have demonstrated to impair memory function heighten susceptibility disorders. Furthermore, elevated quantities reactive oxygen species (ROS) body, known as oxidative stress, exacerbate illnesses negatively affect learning memory. Neuroprotection prevents neuronal cell death by intervening blocking pathogenetic process that leads cellular malfunction death. Methods: We evaluated several studies WEB SCIENCE, SCOPUS, PubMed. we identified central genes signaling pathways associated with neurogenesis, neural system, neuroplasticity through data mining, a literature review artificial intelligence, an in-silico study. Results: Physical exercise (PE) benefits various physiological systems, including nervous system. beneficial impacts physical activity on cognitive performance, well-being, safeguarding neurons against different brain injuries are research PE is powerful non-pharmacological intervention enhances function, memory, while decreasing likelihood developing Additionally, engaging moderate does not result extreme fatigue impact reducing inflammation promoting antioxidant effects. According hormesis theory, inactivity overtraining can decrease function. Conclusions: In summary, combination aerobic exercise, HIIT, resistance training, performed at appropriate intensities, most for neuroprotection health. Regular engagement these activities help mitigate risk diseases enhance overall

Language: Английский

Mechanisms of astrocytic and microglial purinergic signaling in homeostatic regulation and implications for neurological disease DOI Creative Commons
Moawiah M. Naffaa

Exploration of neuroscience, Journal Year: 2025, Volume and Issue: unknown

Published: March 11, 2025

Purinergic signaling, mediated by ATP and adenosine receptors, plays a crucial role in cellular communication homeostasis within the central nervous system (CNS), particularly regulating synaptic activity, glial cell functions, neuroplasticity. Glial cells, including astrocytes microglia, contribute to both short-term processes, such as neurotransmission neuroinflammation, long-term remodeling, tissue repair, behavioral adaptation. Dysregulation of purinergic signaling these cells has been implicated pathogenesis various neurodegenerative neuropsychiatric disorders. This article explores evolving concept synapse, highlighting active modulation emphasizing significance function responses conditions injury neurotoxicity. Specifically, it examines roles receptors—such P2X4, P2X7, P2Y1, P2Y12—in mediating key astrocytic microglial phagocytosis, plasticity, neuronal damage. Furthermore, discusses involvement receptors neurological disorders epilepsy, Alzheimer’s disease, Parkinson’s multiple sclerosis, ischemic stroke, Rett syndrome, autism spectrum disorder, well potential therapeutic strategies targeting mitigate inflammation, promote improve clinical outcomes.

Language: Английский

Citations

0
Editorial: The role of inflammation in neurodegenerative and psychiatric disorders DOI Creative Commons
Dirk M. Hermann,

Mingyue Zhang,

Anfei Huang

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2025, Volume and Issue: 19

Published: March 11, 2025

Inflammation plays a pivotal role in the pathogenesis of neurodegenerative disorders, such as ischemic stroke and Alzheimer's disease, psychiatric namely anxiety depression. Neuroinflammatory responses contribute to neuronal loss diseases 1,2,3 . In stroke, fatigue, depression have been described part cognitive deficits sickness behavior, which unlike focal neurological are strongly dependent on cytokine levels 4 Subtle neuroinflammation associated with activation indoleamine-2,3 dioxygenase-1 pathway is central hallmark major depressive disorder 5 Brain inflammatory predispose oxidative stress, neurotransmitter dysbalance, growth outgrowth disturbances synaptic plasticity disorders 2,3 conditions Targeting neuroinflammatory thus may represent promising way for promoting outcomes both disease groups.Neurodegenerative impose significant health burden, especially older individuals. The association between that develop later life issues often arise during adolescence or middle age supported by epidemiological studies 6 Experimental pointed out associations brain immune surveillance encouraging clinical treatment trials 7,8 Given intricate biology underlying there still numerous critical questions demand attention. It vital elucidate mechanisms enable development new strategies. Therefore, objective this Research Topic was further delve into inflammation diseases, aiming uncover be therapeutically targeted enhancing outcomes. This published four original research papers, illustrate current activities neuroinflammation, neurodegeneration fields an exemplary way. Brain-invading polymorphonuclear neutrophils lymphocytes play key roles injury 1,9 neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte (PLR) lymphocyte-to-monocyte (LMR) peripheral blood previously shown outcome 10,11 , NLR has specifically delirium after 12 article Wang et al. 13 who evaluated 1436 patients without dementia Medical Information Mart Intensive Care (MIMIC)-IV database requiring intensive care unit (ICU) admission, 214 (14.9%) were found delirium. multivariate logistic regression analysis, highest quartile (odds [OR] 2.080, 95% confidence interval [CI], 1.282-3.375) LMR (OR 0.503, CI 0.317-0.798) second PLR 1.574, 1.019-2.431) significantly A restricted cubic spline function showed progressive increase risk higher lower LMR, while Mendelian randomization analysis only negatively data underline relevance leukocyte markers memory disturbances. Future will define molecular mechanisms.Oxidative stress contributor cell damage, via oxidation lipid membranes. Lipoxygenases (LOXs) family lipid-oxidizing enzymes, generate eicosanoids related compounds from arachidonic acid other polyunsaturated fatty acids 14 12/15-LOX special it can directly oxidize membranes containing acids, preceding action phospholipase, leading direct attack organelles 15 presumably underlies cytotoxic activity 12/15-LOX, upregulated neurons endothelial cells their article, Cakir-Aktas 16 exposed mice transient proximal cerebral artery occlusion (MCAo) effect inhibitor ML351 (50 mg/kg) damage. Infarct volume, deficits, peroxidation, pro-inflammatory (interleukin-1β, interleukin-6, tumor necrosis factorα) attenuated inhibition, NOD-like receptor protein (NLRP)-1 -3 signaling non-neuronal These results suggest inhibition suppresses ischemia-induced acute subacute phases suppressing inflammasome activation.Via tripartite synapses, astrocytes transmission 17 Astrocytes involved dysfunction (AD) 18 AD imbalanced cholesterol metabolism, demonstrated high side-chain oxidized known 27-hydroxycholesterol (27-OH), abolish connectivity maturation. Spanos 19 reported downregulation glutamate transporters together increased glial fibrillary acidic hippocampus CYP27Tg mice, mouse model oxysterol dysbalance. Glutamate transporter-1 (GLT-1) also observed when wildtype fed high-cholesterol diets. To study relationship neurons, 3D co-culture system used, reproduced effects 27-OH 2D vivo Moreover, authors novel degenerative did not appear cultures, GLT-1 glutamate-aspartate transporter (GLAST) proposed dysregulation leads hyperexcitability dysfunction. Taken together, these report mechanism linking imbalance through astrocyte function.GATA1 member GATA transcription factor hematopoietic 20 GATA1 dorsolateral prefrontal cortex suffering depression, where act transcriptional repressor synapse-related genes 21 Building upon earlier works, Choi 22 investigated how globally altered gene expression using multi-omics approaches. Through combined analyses ChIPseq, mRNAseq, small RNAseq, profiled potentially affected cultured cortical Gene Ontology revealed might immune-related functions Hypothesizing induces activation, detrimental including synapse depressive-like first performed microglial morphometric overexpressing brains. Fractal ramification process length microglia decreased brains exhibiting overexpression, suggesting increases flow cytometry immunohistochemical activated phenotypes characterized CD86 CD68 Finally, they overexpression behavior could blocked inhibiting show centrally GATA1's behavior.This provides take home messages: (1) Peripheral responses, neutrophil, lymphocyte platelet counts, valuable predictors allow identification developing (2) Lipoxygenases, post-ischemic damage NLRP-1 -3-dependent activation. (3) decreases GLT1 GLAST astrocytes, evokes neuronal-astrocyte co-cultures. (4) behavior. Together, papers emphasize interplay diverse types (neurons, microglia, leukocytes) degenerating brain, maintain injury, most notably membrane structures, disturb integrity function. With respect processes, share surprisingly large number mechanisms. if treatments suitable one area similar application another one. foster translation psychiatry fields.

Language: Английский

Citations

0
Differential Neurogenesis Status Among Achalasia Subtypes DOI Open Access
Qianjun Zhuang, Niandi Tan,

Xun Hou

et al.

Neurogastroenterology & Motility, Journal Year: 2025, Volume and Issue: unknown

Published: March 11, 2025

Achalasia is an acquired esophageal neurodegenerative disorder, characterized by selective loss of inhibitory neurons in the myenteric plexus lower sphincter (LES). The Enteric neural precursor cell (ENPC) essential maintaining neurogenesis, but its role achalasia pathogenesis unknown. This study aimed to explore neurogenesis status LES among patients. specimens from 59 patients with who underwent peroral endoscopic myotomy (POEM) and 19 controls cancer were examined. Double-labeled immunofluorescence staining was performed evaluate Nestin-expressing ENPC axonal innervation LES. Immunofluorescence values compared between groups correlated clinical variables, including demographics, disease duration, Eckardt score, manometric parameters, treatment outcome. A significant reduction Nestin-positive cells, PGP9.5- nNOS-labeled axon observed achalasia. number cells significantly innervation, confirming their roles neurogenesis. immature total axons (Nestin+PGP9.5+) nitrergic (Nestin+nNOS+) different subtypes. Type 2 exhibited a more severe both while type 1 retained axons, depletion mature (Nestin-nNOS+). Neurogenesis generally impaired achalasia; however, varies across subtypes, suggesting that pathophysiology each subtype may be distinct.

Language: Английский

Citations

0
Extracellular vesicles lay the ground for neuronal plasticity by restoring mitochondrial function, cell metabolism and immune balance DOI
Dirk M. Hermann, Chen Wang, Ayan Mohamud Yusuf

et al.

Journal of Cerebral Blood Flow & Metabolism, Journal Year: 2025, Volume and Issue: unknown

Published: March 12, 2025

Extracellular vesicles (EVs) convey complex signals between cells that can be used to promote neuronal plasticity and neurological recovery in brain disease models. These EV are multimodal context-dependent, making them unique therapeutic principles. This review analyzes how EVs released from various cell sources control metabolic function, survival plasticity. Preferential sites of communication the interfaces pre- postsynaptic neurons at synapses, astrocytes plasma membranes or tripartite oligodendrocytes axons, microglial cells/macrophages neurons, cerebral microvascular neurons. At each these interfaces, support mitochondrial function metabolism under physiological conditions orchestrate response injury. In injured brain, promotion by is tightly linked with actions on metabolism, oxidative stress immune responses. Via stabilization balance, responses activated functional induced. As such, lay ground for

Language: Английский

Citations

0
Neuroglia and extracellular matrix molecules DOI
Egor Dzyubenko, Dirk M. Hermann

Handbook of clinical neurology, Journal Year: 2025, Volume and Issue: unknown, P. 197 - 211

Published: Jan. 1, 2025

Language: Английский

Citations

0
Aggression as a contributing factor to social defeat and stress vulnerability DOI Creative Commons

Molykutty John,

Michael Pratt, Jazmine D.W. Yaeger

et al.

Neurobiology of Stress, Journal Year: 2025, Volume and Issue: unknown, P. 100728 - 100728

Published: April 1, 2025

Language: Английский

Citations

0
The neuroplastic brain: current breakthroughs and emerging frontiers DOI Creative Commons
Parisa Gazerani

Brain Research, Journal Year: 2025, Volume and Issue: unknown, P. 149643 - 149643

Published: April 1, 2025

Language: Английский

Citations

0
Postmortem evidence of microglial involvement in the child abuse-associated increase of perineuronal nets in the ventromedial prefrontal cortex DOI Creative Commons
Claudia Belliveau, Reza Rahimian, Gohar Fakhfouri

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: March 13, 2024

Abstract Microglia, known for their diverse roles in the central nervous system, have recently been recognized involvement degrading extracellular matrix. Perineuronal nets (PNNs), a specialized form of this matrix, are crucial stabilizing neuronal connections and constraining plasticity. Our group reported increased PNN densities ventromedial prefrontal cortex (vmPFC) depressed individuals that died by suicide adulthood after experiencing childhood abuse (DS-CA) compared to matched controls. To explore potential underlying mechanisms, we employed comprehensive approach similar postmortem vmPFC samples, combining human matrix metalloproteinase chemokine array, isolation CD11b-positive microglia enzyme-linked immunosorbent assays (ELISA). findings indicate significant downregulation (MMP)-9 tissue inhibitors metalloproteinases (TIMP)-2 both whole grey matter isolated microglial cells from DS-CA samples. Furthermore, our experiments reveal history child is associated with diminished levels CX3CR1 IL33R lysate CD11b cells. However, ligand, CX3CL1 (Fractalkine), did not differ between groups. While these data suggest long-lasting alterations markers exposed severe adversity, direct functional assessments were conducted. Nonetheless, offer insight into how may contribute via microglial-related mechanisms. Graphical

Language: Английский

Citations

3
Microglia Signaling in Health and Disease – Implications in Sex-Specific Brain Development and Plasticity DOI
Subrata Pramanik,

Hyde Thomas M,

Saswata Chakrabarty

et al.

Neuroscience & Biobehavioral Reviews, Journal Year: 2024, Volume and Issue: 165, P. 105834 - 105834

Published: July 29, 2024

Language: Английский

Citations

2
The therapeutic potential of traditional Chinese medicine in depression: focused on the modulation of neuroplasticity DOI Creative Commons
Shimeng Lv,

Ni Yang,

Yitong Lu

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15

Published: Aug. 26, 2024

Depression, a mood disorder characterized by persistent low and lack of enjoyment, is considered the leading cause non-fatal health losses worldwide. Neuroplasticity refers to brain’s ability adapt external or internal stimuli, resulting in functional structural changes. This process plays crucial role development depression. Traditional Chinese Medicine (TCM) shows significant potential as complementary alternative therapy for neurological diseases, including However, there has been no systematic summary neuroplasticity pathological depression TCM Interventions currently. review systematically summarized recent literature on changes analyzed regulatory mechanisms active metabolites formulas antidepressant treatment. Additionally, this discussed limitations current research application prospects regulating research.

Language: Английский

Citations

2