
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Год журнала: 2023, Номер 1870(3), С. 166992 - 166992
Опубликована: Дек. 19, 2023
Язык: Английский
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Год журнала: 2023, Номер 1870(3), С. 166992 - 166992
Опубликована: Дек. 19, 2023
Язык: Английский
Frontiers in Neuroscience, Год журнала: 2023, Номер 17
Опубликована: Март 20, 2023
Autism spectrum disorder (ASD) is a common neurodevelopmental with onset in childhood. The mechanisms underlying ASD are unclear. In recent years, the role of microglia and astrocytes has received increasing attention. Microglia prune synapses or respond to injury by sequestrating site expressing inflammatory cytokines. Astrocytes maintain homeostasis brain microenvironment through uptake ions neurotransmitters. However, molecular link between and, remains unknown. Previous research shown significant ASD, reports increased numbers reactive postmortem tissues animal models ASD. Therefore, an enhanced understanding roles essential for developing effective therapies. This review aimed summarize functions their contributions
Язык: Английский
Процитировано
46Theranostics, Год журнала: 2023, Номер 13(10), С. 3434 - 3450
Опубликована: Янв. 1, 2023
Background: Alzheimer's disease (AD), one of the most common forms dementia, is a widely studied neurodegenerative characterized by Aβ accumulation and tau hyperphosphorylation. Currently, there no effective cure available for AD.The astrocyte AQP4 polarized distribution-mediated glymphatic system essential abnormal clearance potential therapeutic target AD.However, role exercise on distribution association between phenotype polarization are poorly understood.Methods: Using streptozotocin (STZ)-induced sporadic AD rat model, we investigated effects high-intensity interval training pathologies.The Branes maze task was conducted to measure spatial learning memory.Immunofluorescence staining NeuN with TUNEL, Fluoro-Jade C, relative neuronal damage markers applied apoptosis, neurodegeneration, damage.Sholl analysis carried out analyze morphology microglia.Line-scan analysis, 3D rendering, orthogonal view were colocalization.Western blot enzyme-linked immunosorbent assay (ELISA) examine Aβ, respectively.An APP/PS1 transgenic mice model used confirm key findings.Results: High-intensity (HIIT) alleviates cognitive dysfunction in STZ-induced AD-like models provides neuroprotection against damage, loss.Additionally, HIIT improved drainage from cortex hippocampus via kidney.Further mechanistic studies support that beneficial might be due, part, glial cells neurotoxic towards neuroprotective phenotype.Furthermore, an intriguing finding our study strongly correlated phenotype.We found A2 exhibited more evident than A1 phenotype. Conclusion:Our findings indicate ameliorates disease-like pathology regulating phenotype-associated polarization.These changes promote p-tau brain tissue through kidney.
Язык: Английский
Процитировано
45Cell & Bioscience, Год журнала: 2022, Номер 12(1)
Опубликована: Июнь 17, 2022
Major depressive disorder is characterized by not only monoamine neurotransmitters deficiencies but also persistent neuroinflammation. The complement system an attractive therapeutic target for various inflammation-related diseases due to its early activation in inflammatory processes.In the present study, dynamic alteration of C3 and receptor C3aR during occurrence depression mechanism astrocyte-microglia IL-1R/C3/C3aR on synaptic pruning were investigated. proteomic analysis firstly showed that chronic stress caused elevation C3. GO indicated system-mediated signaling was involved depression. observation C3/C3aR activated onset throughout course induced lipopolysaccharide (LPS) stress. In contrast, blockade inhibited hyperactivation microglial APT2/DHHC7 palmitoylation cycle, which mediated translocation STAT3 expression proinflammatory cytokines. Meanwhile, attenuated enhanced synaptogenesis prefrontal cortex mice. Moreover, IL-1R/NF-κB pathway reduced release from astrocyte.The current study demonstrates causes abnormal depression, suggests may be particularly helpful predicting stage
Язык: Английский
Процитировано
38Aging and Disease, Год журнала: 2023, Номер unknown, С. 0 - 0
Опубликована: Янв. 1, 2023
Alzheimer’s disease, one of the most common forms dementia, is characterized by a slow progression cognitive impairment and neuronal loss. Currently, approved treatments for AD are hindered various side effects limited efficacy. Despite considerable research, practical have not been developed. Increasing evidence shows that glial cells, especially microglia astrocytes, essential in initiation AD. During progression, activated resident increases ability resting astrocytes to transform into reactive promoting neurodegeneration. Extensive clinical molecular studies show involvement astrocyte-mediated neuroinflammation pathology, indicating may be potential therapeutic targets This review will summarize significant recent advances pathogenesis three parts. First, we typical pathological changes discuss terms function phenotypic changes. Second, describe astrocytes’ physiological role These roles include inflammatory response, “eat me” “don’t eat signals, Aβ seeding, propagation, clearance, synapse loss, synaptic pruning, remyelination, demyelination. Last, pharmacological non-pharmacological therapies targeting We conclude development Therefore, understanding new critical future trials. Moreover, pharmacological, with specific investigating damage repair, promising research direction regarding treatment prevention.
Язык: Английский
Процитировано
27International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(9), С. 8451 - 8451
Опубликована: Май 8, 2023
Epilepsy is a challenging brain disorder that often difficult to treat with conventional therapies. The gut microbiota has been shown play an important role in the development of neuropsychiatric disorders, including epilepsy. In this study, effects Bifidobacterium longum, probiotic, on inflammation, neuronal degeneration, and behavior are evaluated lithium-pilocarpine model temporal lobe epilepsy (TLE) induced young adult rats. B. longum was administered orally at dose 109 CFU/rat for 30 days after pilocarpine injection. results show treatment beneficial TLE-induced changes anxiety levels, death amygdala, body weight recovery. addition, increased expression anti-inflammatory neuroprotective genes, such as Il1rn Pparg. However, probiotic had little effect astrogliosis microgliosis did not reduce hippocampus cortex. study suggests may have TLE provide valuable insights into bacteria epileptogenesis. be promising drug comprehensive
Язык: Английский
Процитировано
23International Journal of Molecular Medicine, Год журнала: 2024, Номер 53(5)
Опубликована: Апрель 2, 2024
Chronic neuroinflammation serves a key role in the onset and progression of neurodegenerative disorders. Mitochondria serve as central regulators neuroinflammation. In addition to providing energy cells, mitochondria also participate immunoinflammatory response disorders including Alzheimer's disease, Parkinson's multiple sclerosis epilepsy, by regulating processes such cell death inflammasome activation. Under inflammatory conditions, mitochondrial oxidative stress, epigenetics, dynamics calcium homeostasis imbalance may underlying regulatory mechanisms for these diseases. Therefore, investigating related dysfunction result therapeutic strategies against chronic neurodegeneration. The present review summarizes neuroinflammatory diseases current treatment approaches that target
Язык: Английский
Процитировано
15Anatomical Science International, Год журнала: 2024, Номер unknown
Опубликована: Май 13, 2024
Abstract Traumatic brain injuries (TBI) commonly occur following head trauma. TBI may result in short- and long-term complications which lead to neurodegenerative consequences, including cognitive impairment post-TBI. When investigating the neurodegeneration TBI, studies have highlighted role reactive astrocytes neuroinflammation degeneration process. This review showcases a variety of markers that show astrocyte presence under pathological conditions, glial fibrillary acidic protein (GFAP), Crystallin Alpha-B (CRYA-B), Complement Component 3 (C3) S100A10. Astrocyte activation white-matter inflammation, expressed as hyperintensities. Other changes include increased cortical thickness white matter. addresses gaps literature regarding post-mortem human focussing on astrocytes, alongside potential uses these proteins future investigate proportions post-TBI has been discussed. research benefit focus play assist clinicians managing patients who suffered TBI.
Язык: Английский
Процитировано
11Cells, Год журнала: 2024, Номер 13(11), С. 921 - 921
Опубликована: Май 27, 2024
The astrocyte population, around 50% of human brain cells, plays a crucial role in maintaining the overall health and functionality central nervous system (CNS). Astrocytes are vital orchestrating neuronal development by releasing synaptogenic molecules eliminating excessive synapses. They also modulate excitability contribute to CNS homeostasis, promoting survival clearance neurotransmitters, transporting metabolites, secreting trophic factors. highly heterogeneous respond injuries diseases through process known as reactive astrogliosis, which can both inflammation its resolution. Recent evidence has revealed remarkable alterations transcriptomes response several diseases, identifying at least two distinct phenotypes called A1 or neurotoxic A2 neuroprotective astrocytes. However, due vast heterogeneity these it is limited classify them into only phenotypes. This review explores various physiological pathophysiological roles, potential markers, pathways that might be activated different astrocytic Furthermore, we discuss main neurodegenerative identify therapeutic strategies. Understanding underlying mechanisms differentiation imbalance population will allow identification specific biomarkers timely approaches diseases.
Язык: Английский
Процитировано
9Frontiers in Medicine, Год журнала: 2025, Номер 11
Опубликована: Янв. 7, 2025
Human immunodeficiency virus (HIV) infection is the cause of acquired syndrome (AIDS). Combination antiretroviral therapy (cART) has successfully controlled AIDS, but HIV-associated neurocognitive disorders (HANDs) remain prevalent among people with HIV. HIV often associated substance use, which promotes transmission and viral replication exacerbates HANDs even in era cART. Thus, comorbid effects use exacerbate neuropathogenesis HANDs. Unraveling mechanism(s) this exacerbation at molecular, cell-type, brain region levels may provide a better understanding HAND persistence. This review aims to highlight specific regions cell types involved persistence includes an overview post-translational modifications, alterations microglia-specific biomarkers, possible mechanistic pathways that link epigenomic modifications functional protein microglia. The impairment microglial proteins are neural circuit function appears contribute breakdown cellular communication neurodegeneration epigenetic modification N-terminal acetylation currently understudied, discussed brief demonstrate important role infected microglia within regions. discussion also explores whether combined effective preventing or substance-use-mediated
Язык: Английский
Процитировано
1International Journal of Molecular Sciences, Год журнала: 2022, Номер 23(9), С. 4995 - 4995
Опубликована: Апрель 30, 2022
Astrocytes, as the most abundant glial cells in central nervous system, are tightly integrated into neural networks and participate numerous aspects of brain physiology pathology. They main homeostatic loss astrocyte physiological functions and/or gain pro-inflammatory functions, due to their reactivation or cellular senescence, can have profound impacts on surrounding microenvironment with pathological outcomes. Although importance astrocytes is generally recognized, both senescence reactive astrogliosis been extensively reviewed independently, there only a few comparative overviews these complex processes. In this review, we summarize latest data regarding outline similarities differences between phenotypes from morphological, functional, molecular points view. A special focus has given neurodegenerative diseases, where phenotypic alternations significantly implicated. We also current perspectives new advances model systems based well pointing potential therapeutic targets.
Язык: Английский
Процитировано
28