H
Herbert Budka
Researcher at University of Zurich
Publications - 417
Citations - 26786
Herbert Budka is an academic researcher from University of Zurich. The author has contributed to research in topics: Neuropathology & PRNP. The author has an hindex of 85, co-authored 412 publications receiving 25100 citations. Previous affiliations of Herbert Budka include Medical University of Vienna & University of Pécs.
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Journal ArticleDOI
Glial fibrillary acidic protein and S-100 protein in human hepatic encephalopathy: immunocytochemical demonstration of dissociation of two glia-associated proteins.
T. Kimura,Herbert Budka +1 more
TL;DR: A clear dissociation between GFAP and S100P defines Alzg II as a peculiar glial reaction with a rather selective deficit of GFAP metabolism (“gliofibrillary dystrophy”).
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Fibulin-5 mutations link inherited neuropathies, age-related macular degeneration and hyperelastic skin.
Michaela Auer-Grumbach,Martin Weger,Regina Fink-Puches,Lea Papić,Eleonore Fröhlich,Piet Auer-Grumbach,Laila El Shabrawi-Caelen,Maria Schabhüttl,Christian Windpassinger,Jan Senderek,Herbert Budka,Slave Trajanoski,Andreas R. Janecke,Anton Haas,Dieter Metze,Thomas R. Pieber,Christian Guelly +16 more
TL;DR: Fructose-5 is identified as a gene involved in Charcot-Marie-Tooth neuropathies and heterozygous fibulin-5 mutations are revealed in 2% of patients with age-related macular degeneration, which adumbrates a new syndrome by linking concurrent pathologic alterations affecting peripheral nerves, eyes and skin to mutations in the fibulin -5 gene.
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A New Mechanism for Transmissible Prion Diseases
Natallia Makarava,Gabor G. Kovacs,Regina Savtchenko,Irina Alexeeva,Valeriy G. Ostapchenko,Valeriy G. Ostapchenko,Herbert Budka,Robert G. Rohwer,Ilia V. Baskakov +8 more
TL;DR: This study provides compelling evidence that noninfectious amyloids with a structure different from that of PrPSc could lead to transmissible prion disease and has numerous implications for understanding the etiology of prion and other neurodegenerative diseases.
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Suprasellar meningioma with expression of glial fibrillary acidic protein: a peculiar variant
Julia Wanschitz,Manfred Schmidbauer,Hans Maier,Hans Maier,Karl Rössler,Peter Vorkapic,Herbert Budka +6 more
TL;DR: A 24-year-old female presented with a 3-year history of a suprasellar and intraventricular solid midline process measuring about 3×4 cm, which most likely represents a peculiar variant of meningioma with prominent production of GFAP, as previously described.
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Prominent cortical atrophy with neuronal loss as correlate of human immunodeficiency virus encephalopathy.
TL;DR: The presentation of a 25-year-old homosexual AIDS patient with progressive cognitive, motor and behavioral disturbances consistent with HIV encephalopathy suggests that HIV infection of the brain may cause predominant cortical nerve cell loss, and that HIVEncephalopathy is not necessarily due to white matter lesions.