Image 1.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10921325 | PMC |
| http://dx.doi.org/10.1016/j.jpha.2023.10.002 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Kaempferol attenuates experimental autoimmune neuritis through TNFR1/JNK/p38 signaling pathway inhibition.
Int Immunopharmacol
January 2025
Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan 750004, China; Diagnosis and Treatment Engineering Technology Research Center of Nervous System Diseases of Ningxia, Yinchuan 750004, China; Neurology Center, General Hospital of Ningxia Medical University, Yinchuan 750004, China. Electronic address:
Kaempferol (Kae) is a flavonoid that has antioxidant, anti-inflammatory and neuroprotective effects. In recent years, there have been increasing reports on viral infection-induced Guillain-Barré syndrome (GBS) with high rates of disability and fatality. Therefore, in order to search for effective peripheral nerve injury repair drugs, we used rats with experimental autoimmune neuritis (EAN) as the typical animal model for GBS, and implemented Kae treatment intervention on EAN rats.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
School of Medical & Allied Sciences, K.R. Mangalam University, Gurugram, Haryana, India.
Background: Parkinson's disease is a hypokinetic disorder characterized by selective loss of dopaminergic in substantia nigra pars compacta (SNPc) region of mid-brain. Dopaminergic degeneration of neurons is considered to be due to oxidative stress, neuroinflammation, neurons mitochondrial dysfunction and glutamate excitotoxicity etc. Inosine a purine nucleoside has been reported to produce anti-oxidant, anti-inflammatory and neuromodulatory actions in previous studies.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University Institute of Pharmaceutical sciences, Panjab University, Chandigarh, Chandigarh, India.
Background: Traumatic brain injury (TBI) due to external forces is a major cause of morbidity and mortality among people of all age groups, worldwide. Multiple biological processes like neuroinflammation, mitochondrial dysfunction, oxidative stress, amyloid β (Aβ) production, and tau hyperphosphorylation are involved in the pathogenesis of TBI. The role of neuroinflammation and oxidative stress has been suggested in the pathophysiology of brain injury-induced cognitive dysfunction.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Medical University of South Carolina, Charleston, SC, USA.
Background: Alzheimer's disease (AD) is associated with cognitive impairment and neuro-inflammation. Dysregulated activation of microglia and astrocytes induces neuro-inflammation, and reactive astrocytes have been classified into A1 neurotoxic and A2 neuroprotective phenotypes. A1 astrocytes are induced by activated neuro-inflammatory microglia via secreting IL-1α, TNFα and C1q, and contributing to inflammation and neuronal cell death.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Byrd Alzheimer's Center & Research Institute, Tampa, FL, USA.
Background: BIN1, the second strongest GWAS risk factor for late-onset Alzheimer's disease (AD), encodes a nucleocytoplasmic adaptor protein that plays many roles in multiple tissue and cell types. It is known that BIN1 can directly bind to tau in vitro, and neuronal BIN1 expression decreases in patients with AD. Accumulation of intracellular hyperphosphorylated tau is a hallmark pathogenic feature of AD and related tauopathies.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!