Progressive supranuclear palsy (PSP) is a neurodegenerative disease based on four-repeat tauopathy pathology. Currently, this entity is not fully recognized in the context of pathogenesis or clinical examination. This review evaluates the association between neuroinflammation and microglial activation with the induction of pathological cascades that result in tauopathy pathology and the clinical manifestation of PSP. Multidimensional analysis was performed by evaluating genetic, biochemical, and neuroimaging biomarkers to determine whether neurodegeneration as an effect of neuroinflammation or neuroinflammation is a consequence of neurodegeneration in PSP. To the best of our knowledge, this review is the first to investigate PSP in this context.
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http://dx.doi.org/10.3389/fnins.2020.00893 | DOI Listing |
J Neuroinflammation
January 2025
Department of Neurology, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Yishan Road 600, Shanghai, 200233, China.
Background: Alzheimer's disease (AD) is a prevalent neurodegenerative disorder worldwide, and microglia are thought to play a central role in neuroinflammatory events occurring in AD. Chemerin, an adipokine, has been implicated in inflammatory diseases and central nervous system disorders, yet its precise function on microglial response in AD remains unknown.
Methods: The APP/PS1 mice were treated with different dosages of chemerin-9 (30 and 60 µg/kg), a bioactive nonapeptide derived from chemerin, every other day for 8 weeks consecutively.
NPJ Parkinsons Dis
January 2025
Department of Neurobiology, Center of Parkinson Disease Beijing Institute for Brain Disorders, Beijing Key Laboratory on Parkinson Disease, Key Laboratory for Neurodegenerative Disease of the Ministry of Education, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, Beijing, 100069, China.
Chronic neuroinflammation with sustained microglial activation occurs in Parkinson's disease (PD), yet the mechanisms and exact contribution of these cells to the neurodegeneration remains poorly understood. In this study, we induced progressive dopaminergic neuron loss in mice via rAAV-hSYN injection to cause the neuronal expression of α-synuclein, which produced neuroinflammation and behavioral alterations. We administered PLX5622, a colony-stimulating factor 1 receptor inhibitor, for 3 weeks prior to rAAV-hSYN injection, maintaining it for 8 weeks to eliminate microglia.
View Article and Find Full Text PDFPhytomedicine
December 2024
Department of Psychiatry and Psychotherapy, University Medical Center Mainz, Johannes Gutenberg-University Mainz, Mainz, Germany; Research Center for Immunotherapy (FZI), University Medical Center at the Johannes Gutenberg University Mainz, Mainz, Germany. Electronic address:
Background: Ginkgo biloba leaf extract EGb 761® has shown clinical efficacy in patients with mild cognitive impairment and dementia. However, the pharmacological action of EGb 761® in Alzheimer's disease (AD) remains unclear and molecular mechanisms targeted in the brain are not completely understood.
Hypothesis/purpose: We aimed to investigate 1) the potential sex-dependent effects of oral administration of EGb 761® in 5xFAD mice, an AD mouse model, and 2) the underlying microglial subtype responsible for the observed anti-inflammatory effects in the brain.
CNS Neurol Disord Drug Targets
January 2025
Department of Pharmacy, Teerthanker Mahaveer College of Pharmacy, Teerthanker Mahaveer University, Moradabad (UP)-244001, India.
Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by social communication deficits and repetitive behaviors. Emerging evidence highlights the significant role of glial cells, particularly astrocytes and microglia, in the pathophysiology of ASD. Glial cells are crucial for maintaining homeostasis, modulating synaptic function, and responding to neural injury.
View Article and Find Full Text PDFPharmaceuticals (Basel)
December 2024
Department of Anesthesiology, Cathay General Hospital, Taipei 106, Taiwan.
Background: Morphine analgesic tolerance (MAT) limits the clinical application of morphine in the management of chronic pain. IIK7 is a melatonin type 2 (MT2) receptor agonist known to have antioxidant properties. Oxidative stress is recognized as a critical factor in MAT.
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