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Behavioural Brain Research|July 5, 2026
Behavioral characterization of bulbar sensorimotor function in a rat model of Alexander diseaseJared Cullen, John Russell, Cynthia A Kelm-Nelson, et al.Development (Cambridge, England)|June 10, 2005
PTEN deletion in Bergmann glia leads to premature differentiation and affects laminar organizationQing Yue, Matthias Groszer, Jose S Gil, et al.Journal of Neuroinflammation|March 9, 2021
Pexidartinib treatment in Alexander disease model mice reduces macrophage numbers and increases glial fibrillary acidic protein levels, yet has minimal impact on other disease phenotypesMichelle M Boyd, Suzanne J Litscher, Laura L Seitz, et al.The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|February 11, 2005
Transgenic expression of human connexin32 in myelinating Schwann cells prevents demyelination in connexin32-null miceSteven S Scherer, Yi-Tian Xu, Albee Messing, et al.Plos One|September 18, 2015
Lithium Decreases Glial Fibrillary Acidic Protein in a Mouse Model of Alexander DiseaseChristine M LaPash Daniels, Elizabeth Paffenroth, Elizabeth V Austin, et al.Human Molecular Genetics|July 15, 2005
Gene expression analysis in mice with elevated glial fibrillary acidic protein and Rosenthal fibers reveals a stress response followed by glial activation and neuronal dysfunctionTracy L Hagemann, Stephen A Gaeta, Mark A Smith, et al.Annals of Neurology|December 12, 2017
Antisense suppression of glial fibrillary acidic protein as a treatment for Alexander diseaseTracy L Hagemann, Berit Powers, Curt Mazur, et al.The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|February 2, 2022
Anastasis Drives Senescence and Non-Cell Autonomous Neurodegeneration in the Astrogliopathy Alexander DiseaseLiqun Wang, Hassan Bukhari, Linghai Kong, et al.The Journal of Biological Chemistry|February 5, 2002
Genetic analysis of the mammalian K+ channel beta subunit Kvbeta 2 (Kcnab2)Ken McCormack, Jolien X Connor, Lei Zhou, et al.ASN Neuro|February 21, 2012
Neurological diseases as primary gliopathies: a reassessment of neurocentrismAlexei Verkhratsky, Michael V Sofroniew, Albee Messing, et al.Pageof 17