• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

The small molecule inhibitor PR-619 protects retinal ganglion cells against glutamate excitotoxicity
This study was designed to investigate the role of PR-619 in regulating mitophagy of RGCs under glutamate excitotoxicity. Primary cultured RGCs were incubated with PR-619 or vehicle control in the excitotoxicity model of 100 µM glutamate treatment. Mitochondrial membrane potential was assessed by JC-1 assay. Cytotoxicity of RGCs was measured by LDH activity. Proteins levels of parkin, optineurin, LAMP1, Bax, Bcl-2 and the LC3-II/I ratio were analyzed by western blot. The distribution and morphology of mitochondria in RGCs was stained by MitoTracker and antibody against mitochondria membrane protein, and examined by confoc...
Source: NeuroReport - October 6, 2020 Category: Neurology Tags: Degeneration and Repair Source Type: research

Brain Dicer1 Is Down-Regulated in a Mouse Model of Alzheimer ’s Disease Via Aβ42-Induced Repression of Nuclear Factor Erythroid 2-Related Factor 2
This study may open new avenues for investigating potential pathognomonics and pathogenesis in AD.
Source: Molecular Neurobiology - September 24, 2020 Category: Neurology Source Type: research

Functional Regulation of an Oxidative Stress Mediator, Rac1, in Diabetic Retinopathy
AbstractPurposeEarly activation of cytosolic NADPH oxidase-2 (Nox2) in diabetes increases retinal ROS production, damaging their mitochondria. The assembly of Nox2 holoenzyme requires activation of a small molecular weight G protein Rac1. Rac1 activation is regulated by guanine exchange factors and guanine nucleotide-dissociation inhibitors, and post-translational modifications assist in its association with exchange factors and dissociation inhibitors. The goal of this study is to investigate the mechanisms of Rac1 activation in the development of diabetic retinopathy.MethodsThe levels of the dissociation inhibitor, preny...
Source: Molecular Neurobiology - November 7, 2019 Category: Neurology Source Type: research

snRPN controls the ability of neurons to regenerate axons.
CONCLUSION: These results suggest that coordinated snRPN-driven activities within the neuron-specific ribonucleoprotein complex regulate the regenerative ability of RGCs in primates, thereby highlighting a potential new role for snRPN within neurons and the possibility of novel postinjury therapies. PMID: 29439367 [PubMed - in process]
Source: Restorative Neurology and Neuroscience - February 15, 2018 Category: Neurology Tags: Restor Neurol Neurosci Source Type: research