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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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Glial fibrillary acidic protein and S-100 protein in human hepatic encephalopathy: immunocytochemical demonstration of dissociation of two glia-associated proteins.

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.

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

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

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.