Advancing knowledge of human development, developmental disabilities, and neurodegenerative diseases.
Alexander disease (AxD) is a rare neurological disorder caused by dominant gain-of-function mutations in the gene for glial acidic fibrillary protein (GFAP).
New research from Waisman investigator, Tracy Hagemann, PhD, associate research professor, delves into the cognitive impairments and associated molecular changes caused by Alexander disease (AxD), revealing similarities to other neurodegenerative diseases like Alzheimer’s.
The hallmarks of Alexander disease, aggregation of misfolded GFAP proteins and dysregulation of brain cells called astrocytes, may be stopped and reversed in rodent models with the inactivation of the transcription factor STAT3.
Messing wanted to study if the overexpression of GFAP resulted in a certain reactive response in the brain.
Anastasis is a recently described process in which cells recover after late-stage apoptosis activation. The functional consequences of anastasis for cells and tissues are not clearly understood.
Two Waisman investigators were recently awarded a new professor title track at UW-Madison.
Alexander disease (AxD) is a devastating leukodystrophy caused by gain-of-function mutations in GFAP, and the only available treatments are supportive. Recent advances in antisense oligonucleotide (ASO) therapy have demonstrated that transcript targeting can be a successful strategy for human neurodegenerative diseases amenable to this approach.
Alexander disease is a progressive and rare neurological disorder with no cure or standard course of treatment. But a new study led by researchers at the University of Wisconsin–Madison involving a rat model of the disease offers a potential treatment for the typically fatal condition.
Alexander disease (AxD) is a rare neurodegenerative disorder that is caused by dominant mutations in the gene encoding glial fibrillary acidic protein (GFAP), an intermediate filament that is primarily expressed by astrocytes. In AxD, mutant GFAP in combination with increased GFAP expression result in astrocyte dysfunction and the accumulation of Rosenthal fibers.
Alexander disease results from gain of function mutations in the gene encoding glial fibrillary acidic protein (GFAP). At least eight GFAP isoforms have been described, however, the predominant alpha isoform accounts for approximately 90% of GFAP protein.
