International Immunopharmacology, Journal Year: 2024, Volume and Issue: 146, P. 113816 - 113816
Published: Dec. 20, 2024
Language: Английский
Trends in Neurosciences, Journal Year: 2021, Volume and Issue: 44(9), P. 714 - 727
Published: Aug. 5, 2021
Language: Английский
Citations
168
Theranostics, Journal Year: 2023, Volume and Issue: 13(12), P. 4138 - 4165
Published: Jan. 1, 2023
Neurodegenerative diseases are characterized by the progressive loss of neurons and intricate interactions between different cell types within affected regions.Reliable biomarkers that can accurately reflect disease activity, diagnose, monitor progression neurodegenerative crucial for development effective therapies.However, identifying suitable has been challenging due to heterogeneous nature these diseases, affecting specific subsets in brain regions.One promising approach promoting regeneration recovery involves transplantation mesenchymal stem cells (MSCs).MSCs have demonstrated ability modulate immune system, promote neurite outgrowth, stimulate angiogenesis, repair damaged tissues, partially through release their extracellular vesicles (EVs).MSC-derived EVs retain some therapeutic characteristics parent MSCs, including regulate facilitate tissue repair.This review aims explore potential MSC-derived as an emerging strategy highlighting role modulating neuronal recovery.By elucidating mechanisms which exert effects, we advance our understanding leverage novel treatment approaches field diseases.
Language: Английский
Citations
66
Alzheimer s & Dementia, Journal Year: 2023, Volume and Issue: 20(1), P. 709 - 727
Published: Oct. 9, 2023
Abstract Aging, tau pathology, and chronic inflammation in the brain play crucial roles synaptic loss, neurodegeneration, cognitive decline tauopathies, including Alzheimer's disease. Senescent cells accumulate aging brain, accelerate process, promote tauopathy progression through their abnormal inflammatory secretome known as senescence‐associated secretory phenotype (SASP). Tau oligomers (TauO)—the most neurotoxic species—are to induce senescence SASP, which subsequently neuropathology, inflammation, oxidative stress, dysfunction, neuronal death, dysfunction. TauO, are associated with heterogeneity decline. However, underlying mechanisms driving disease remain largely unknown, impeding development of therapies for tauopathies. Based on clinical preclinical evidence, this review highlights critical role TauO neurodegeneration. We discuss key knowledge gaps potential strategies targeting treat Highlights Senescence, oligomeric (TauO), process contributing highlight target tauopathies while addressing gaps.
Language: Английский
Citations
32
BMC Neurology, Journal Year: 2023, Volume and Issue: 23(1)
Published: June 12, 2023
Abstract Starting from the perspective of an immune-privileged site, our knowledge inflammatory processes within central nervous system has increased rapidly over last 30 years, leading to a rather puzzling picture today. Of particular interest is emergence disease- and injury-specific responses brain, which may form basis for future therapeutic approaches. To advance this important topic, we invite authors contribute research clinical papers Collection “Neuroinflammation Brain Disease”.
Language: Английский
Citations
24
Journal of Neuroinflammation, Journal Year: 2024, Volume and Issue: 21(1)
Published: May 10, 2024
Abstract Traumatic brain injury (TBI) is a chronic and debilitating disease, associated with high risk of psychiatric neurodegenerative diseases. Despite significant advancements in improving outcomes, the lack effective treatments underscore urgent need for innovative therapeutic strategies. The brain-gut axis has emerged as crucial bidirectional pathway connecting gastrointestinal (GI) system through an intricate network neuronal, hormonal, immunological pathways. Four main pathways are primarily implicated this crosstalk, including systemic immune system, autonomic enteric nervous systems, neuroendocrine microbiome. TBI induces profound changes gut, initiating unrestrained vicious cycle that exacerbates axis. Alterations gut include mucosal damage malabsorption nutrients/electrolytes, disintegration intestinal barrier, increased infiltration cells, dysmotility, dysbiosis, enteroendocrine cell (EEC) dysfunction disruption (ENS) (ANS). Collectively, these further contribute to neuroinflammation neurodegeneration via gut-brain In review article, we elucidate roles various anti-inflammatory pharmacotherapies capable attenuating dysregulated inflammatory response along TBI. These agents hormones such serotonin, ghrelin, progesterone, ANS regulators beta-blockers, lipid-lowering drugs like statins, flora modulators probiotics antibiotics. They attenuate by targeting distinct both post-TBI. exhibit promising potential mitigating inflammation enhancing neurocognitive outcomes patients.
Language: Английский
Citations
12
EClinicalMedicine, Journal Year: 2025, Volume and Issue: 80, P. 103023 - 103023
Published: Jan. 2, 2025
Language: Английский
Citations
1
European Journal of Neuroscience, Journal Year: 2022, Volume and Issue: 57(2), P. 400 - 418
Published: Dec. 10, 2022
Traumatic brain injury (TBI) can be a devastating and debilitating disease to endure. Due improvements in clinical practice, declining mortality rates have led research into the long-term consequences of TBI. For example, incidence severity TBI been associated with an increased susceptibility developing neurodegenerative disorders, such as Parkinson's or Alzheimer's disease. However, mechanisms linking this alarming association are yet fully understood. Recently, there has groundswell evidence implicating microbiota-gut-brain axis pathogenesis these diseases. Interestingly, survivors often report gastrointestinal complaints animal studies demonstrated dysfunction dysbiosis following injury. Autonomic dysregulation chronic inflammation appear main driver pathologies. Consequently, review will explore potential role development diseases
Language: Английский
Citations
28
Journal of Neuroinflammation, Journal Year: 2024, Volume and Issue: 21(1)
Published: April 5, 2024
Abstract Background It is well established that traumatic brain injury (TBI) causes acute and chronic alterations in systemic immune function changes contribute to posttraumatic neuroinflammation neurodegeneration. However, how TBI affects bone marrow (BM) hematopoietic stem/progenitor cells chronically what extent such may negatively impact innate immunity neurological has not been examined. Methods To further understand the role of BM cell derivatives on outcome, we generated chimeric mice by transplanting from injured or sham (i.e., 90 days post-surgery) congenic donor into otherwise healthy, age-matched, irradiated CD45.2 C57BL/6 (WT) hosts. Immune were evaluated flow cytometry, multiplex ELISA, NanoString technology. Moderate-to-severe was induced controlled cortical measured using a battery behavioral tests. Results transcriptome lineage − c-Kit + Sca1 (LSK+) mice, including modified epigenetic senescence pathways. After 8 weeks reconstitution, peripheral myeloid TBI→WT showed significantly higher oxidative stress levels reduced phagocytic activity. At eight months after leukopenic, with continued phagocytosis responses, as persistent deficits. Gene expression analysis revealed BM-driven neuropathology respectively. Chimeric subjected at post-reconstitution longer reconstitution periods time post-injury) associated increased microgliosis leukocyte infiltration. Pre-treatment senolytic agent, ABT-263, improved performance aged baseline, although it did attenuate acutely brain. Conclusions activation progressive dysfunction pool, which drives long-term deficits hematopoiesis, immunity, function, altered sensitivity subsequent injury.
Language: Английский
Citations
4
Neurochemistry International, Journal Year: 2024, Volume and Issue: 180, P. 105874 - 105874
Published: Oct. 2, 2024
Language: Английский
Citations
3
Brain Research, Journal Year: 2024, Volume and Issue: 1845, P. 149271 - 149271
Published: Oct. 11, 2024
Language: Английский
Citations
3