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.
Tracy Hagemann
We need to know STAT: Mechanisms behind GFAP accumulation in Alexander disease involve transcription factor STAT3.
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.
Alexander disease: A lifetime’s work in the hope of saving lives
Messing wanted to study if the overexpression of GFAP resulted in a certain reactive response in the brain.
Tracy L. Hagemann, PhD – Slide of the Week
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 named research professors
Two Waisman investigators were recently awarded a new professor title track at UW-Madison.
Tracy Hagemann, PhD – Slide of the Week
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.
Promising treatment for Alexander disease moves from rat model to human clinical trials
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.
Tracy L. Hagemann, PhD – Slide of the Week
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.
Tracy L. Hagemann, PhD & Albee Messing, VMD, PhD – Slide of the Week
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.
Progress made toward treatment for rare, fatal neurological disease
After more than a decade of work, researchers at the University of Wisconsin–Madison’s Waisman Center reported promising results in the lab and in animal models that could set the stage for developing a treatment for Alexander disease, a rare and usually fatal neurological disease with no known cure.