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Michell M Reimer et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 31(49), 18185-18194 (2011-12-14)
Myelinated axons have a distinct protein architecture essential for action potential propagation, neuronal communication, and maintaining cognitive function. Damage to myelinated axons, associated with cerebral hypoperfusion, contributes to age-related cognitive decline. We sought to determine early alterations in the protein
Ying Yu et al.
Journal of neurochemistry, 152(3), 350-367 (2019-11-27)
Microglia are critical in damage/repair processes during ischemic white matter injury (WMI). Voltage-gated proton channel (Hv1) is expressed in microglia and contributes to nicotinamide adenine dinucleotide phosphate oxidase complex-dependent production of reactive oxygen species (ROS). Recent findings have shown that
Devid Damiani et al.
The Journal of comparative neurology, 520(7), 1406-1423 (2011-11-22)
Retinitis pigmentosa (RP) is a family of inherited diseases causing progressive photoreceptor death. Retinal ganglion cells (RGCs) form the biological substrate for various therapeutic approaches designed to restore vision in RP individuals. Assessment of survival and preservation of RGCs in
Jo Anne Stratton et al.
eNeuro, 4(3) (2017-05-18)
Despite its modest capacity for regeneration, peripheral nervous system injury often results in significant long-term disability. Supplementing peripheral nervous system injury with autologous Schwann cells (SCs) may serve to rejuvenate the postinjury environment to enhance regeneration and ultimately improve functional
Chuan Qin et al.
Theranostics, 8(19), 5434-5451 (2018-12-18)
Rationale: Ischemic white matter damage frequently results in myelin loss, accompanied with microglial activation. We previously found that directing microglia towards an anti-inflammatory phenotype provided a beneficial microenvironment and helped maintain white matter integrity during chronic cerebral hypoperfusion. However, the
Christopher D Makinson et al.
Neuron, 93(5), 1165-1179 (2017-02-28)
Voltage-gated sodium channel (VGSC) mutations cause severe epilepsies marked by intermittent, pathological hypersynchronous brain states. Here we present two mechanisms that help to explain how mutations in one VGSC gene, Scn8a, contribute to two distinct seizure phenotypes: (1) hypoexcitation of
Ping Li et al.
eNeuro, 4(3) (2017-07-01)
The GABA-B receptor is densely expressed throughout the brain and has been implicated in many CNS functions and disorders, including addiction, epilepsy, spasticity, schizophrenia, anxiety, cognitive deficits, and depression, as well as various aspects of nervous system development. How one
Jacy L Wagnon et al.
Neurology. Genetics, 3(4), e170-e170 (2017-07-14)
To determine the functional effect of SCN8A missense mutations in 2 children with intellectual disability and developmental delay but no seizures. Genomic DNA was analyzed by next-generation sequencing. SCN8A variants were introduced into the Nav1.6 complementary DNA by site-directed mutagenesis.
Yasmina Manso et al.
Glia, 66(1), 34-46 (2017-07-20)
Chronic cerebral hypoperfusion is a key mechanism associated with white matter disruption in cerebral vascular disease and dementia. In a mouse model relevant to studying cerebral vascular disease, we have previously shown that cerebral hypoperfusion disrupts axon-glial integrity and the
José Javier Miguel-Hidalgo et al.
Scientific reports, 13(1), 16419-16419 (2023-09-30)
Major depressive disorder (MDD) and chronic unpredictable stress (CUS) in animals feature comparable cellular and molecular disturbances that involve neurons and glial cells in gray and white matter (WM) in prefrontal brain areas. These same areas demonstrate disturbed connectivity with
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