Results 221 to 230 of about 2,080,423 (380)

Pretreatment seizure semiology in childhood absence epilepsy

open access: yesNeurology, 2017
S. Kessler   +11 more
semanticscholar   +1 more source

Resilience to Endoplasmic Reticulum Stress Mitigates Membrane Hyperexcitability Underlying Late Disease Onset in a Murine Model of SCA6

open access: yesAnnals of Neurology, EarlyView.
Objective An enduring puzzle in many inherited neurological disorders is the late onset of symptoms despite expression of function‐impairing mutant protein early in life. We examined the basis for onset of impairment in spinocerebellar ataxia type 6 (SCA6), a canonical late‐onset neurodegenerative ataxia which results from a polyglutamine expansion in ...
Haoran Huang   +10 more
wiley   +1 more source

Neurocognitive Profiles in Childhood Absence Epilepsy

open access: yesJournal of Child Neurology, 2017
D. Cheng   +5 more
semanticscholar   +1 more source

From Diagnosis to Disease Staging: Multisite Validation of Cerebrospinal Fluid Molecular Tests in Multiple Sclerosis

open access: yesAnnals of Neurology, EarlyView.
Objective The growing demand for personalized treatment in multiple sclerosis (MS) highlights the need for more precise biomarkers that can outperform magnetic resonance imaging and clinical assessment in patient stratification. Advances in multiplex proteomic technologies suggest that cerebrospinal fluid (CSF) analysis at MS onset may not only improve
Laura Ghezzi   +10 more
wiley   +1 more source

Vagal nerve signals are modulated by spontaneous seizures in Genetic Absence Epilepsy Rats from Strasbourg. [PDF]

open access: yesFront Neurosci
Collard E   +6 more
europepmc   +1 more source

Neuronal networks underlying ictal and subclinical discharges in childhood absence epilepsy. [PDF]

open access: yesJ Neurol, 2023
Kumar A   +5 more
europepmc   +1 more source

Recombinant Human Neuregulin1‐β1 Significantly Reduces Schwannoma Growth in Mice

open access: yesAnnals of Neurology, EarlyView.
rhNRGβ1‐Replacement‐Therapy: Under physiological conditions, NRGβ1 is expressed on axons (in orange), where it activates ERBB2 receptors, facilitating successful nerve regeneration following injury. However, loss of NF2 leads to a reduction in NRGβ1‐expression and increased ErbB2 levels on Schwann cells (in green), which contributes to schwannoma ...
Julia P. Bischoff   +7 more
wiley   +1 more source

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