Article in Annals of clinical and translational neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
7 authors.
Tracy L HagemannWaisman Center, University of Wisconsin-Madison, Madison, Wisconsin, USA.ORCID 0000-0002-0237-9267
Michelle M SonsallaDepartment of Medicine, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Cora LuzinskiWaisman Center, University of Wisconsin-Madison, Madison, Wisconsin, USA.ORCID 0009-0006-9861-6453
Fernando ZacahuaWaisman Center, University of Wisconsin-Madison, Madison, Wisconsin, USA.
David A HarrisWilliam S. Middleton Memorial Veterans Hospital, Madison, Wisconsin, USA.ORCID 0000-0001-5588-1632
Dudley W LammingDepartment of Medicine, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Albee MessingWaisman Center, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Funding
UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
Coordinating and Bioinformatics Unit for the MMPC/DiaCompU24DK076169 · NIDDK · AUGUSTA UNIVERSITY · PI MCINDOE, RICHARD A. · 2006 to 2018
$42.4M
Wisconsin Alzheimer's Disease Research CenterP30AG062715 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI RICHARD J CHAPPELL · 2019 to 2026
$34.5M
Coordinating Unit for DiaCompU24DK115255 · NIDDK · AUGUSTA UNIVERSITY · PI MCINDOE, RICHARD A. · 2017 to 2020
$11.6M
Waisman Center Intellectual and Developmental Disabilities Research CenterP50HD105353 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI Brittany Gail Travers · 2021 to 2026
$8.5M
Patient-derived iPS cells as model systems for AxDP01HD076892 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI NEDERGAARD, MAIKEN · 2014 to 2018
$6.0M
Wisconsin Nathan Shock CenterP30AG092586 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI Rozalyn M. Anderson · 2025 to 2026
$3.8M
Translational analysis of a novel intervention to promote healthy aging.R01AG085898 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI RICKI J COLMAN, Dudley William Lamming · 2024 to 2026
$3.2M
The regulation of health and longevity by branched-chain amino acidsR01AG056771 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI Dudley William Lamming · 2018 to 2026
$3.1M
The regulation of cancer and aging by methionineR01AG084156 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI VINCENT L. CRYNS, JOHN M DENU · 2023 to 2026
$2.5M
The regulation of health and longevity by branched-chain amino acidsRF1AG056771 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI LAMMING, DUDLEY WILLIAM · 2023 to 2023
$2.1M
Astrocyte-synapse interactions in a rat model of Alexander diseaseR01NS110719 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI HAGEMANN, TRACY · 2019 to 2023
$2.1M
BLRD VA I01 BX004031BLRD VA IS1 BX005524Department of SurgeryEunice Kennedy Shriver National Institute of Child Health and Human Development HD076892Eunice Kennedy Shriver National Institute of Child Health and Human Development HD105353NCI NIH HHS CA014520NCI NIH HHS P30 CA014520NIA NIH HHS AG056771NIA NIH HHS AG062715NIA NIH HHS AG081482NIA NIH HHS AG084156NIA NIH HHS AG085898NIA NIH HHS AG088813NIA NIH HHS AG092586NIA NIH HHS AG094153NIA NIH HHS P30 AG062715NIA NIH HHS P30 AG092586NIA NIH HHS R01 AG056771NIA NIH HHS R01 AG084156NIA NIH HHS R01 AG085898NIA NIH HHS R01 AG094153NIA NIH HHS R03 AG088813NIA NIH HHS R56 AG056771NIA NIH HHS RF1 AG056771NIA NIH HHS U01 AG081482NICHD NIH HHS P01 HD076892NICHD NIH HHS P50 HD105353NIDDK NIH HHS DK076169NIDDK NIH HHS DK115255NIDDK NIH HHS DK125859NIDDK NIH HHS R01 DK125859NIDDK NIH HHS U24 DK076169NIDDK NIH HHS U24 DK115255NINDS NIH HHS NS110719NINDS NIH HHS NS136328NINDS NIH HHS R01 NS110719NINDS NIH HHS R56 NS136328University of Wisconsin Carbone Cancer CenterUniversity of Wisconsin-MadisonU.S. Department of Veterans Affairs I01-BX004031U.S. Department of Veterans Affairs IS1-BX005524Wisconsin Partnership Program at the UW School of Medicine and Public Health ID 6770-2024
6 · The paper itself
Abstract
objectiveAlexander disease (AxD) is a severe neurodegenerative disorder caused by gain-of-function mutations in the gene for GFAP, which lead to protein aggregation and a primary astrocytopathy. Symptoms vary, but failure to thrive (FTT) and frequent emesis are common and cause significant morbidity. Here we investigate GDF15, a member of the TGFβ superfamily, which regulates energy balance and appetite, as a potential mediator of FTT in AxD.
methodsIn this study, we use the Gfap
resultsR237H rats show reduced lean and fat mass and muscle atrophy despite reduced energy expenditure, and at an early age exhibit pica and anorexia. GDF15 is expressed by R237H rat astrocytes and is elevated in brainstem and CSF, but not in plasma. Neurons expressing GFRAL, a mediator of GDF15-induced appetite suppression, are activated in the area postrema. Suppression of GFAP using antisense oligonucleotides normalizes weight gain and GDF15 levels in brainstem and CSF. In human AxD, GDF15 is elevated in CSF, but not in blood.
interpretationGDF15 is associated with FTT in AxD and provides both a target and useful biomarker for the development of future therapeutics.
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Growth Differentiation Factor 15 Elevation in the Central Nervous System Is Associated With Failure to Thrive in Alexander Disease. · full record | OpenQuestion