His main research concerns Pathology, Genetics, Biochemistry, Cell biology and Disease. His Pathology research includes elements of Epitope and Magnetic resonance imaging. Armin Giese interconnects Virology and Fatal familial insomnia in the investigation of issues within Genetics.
His research integrates issues of Creutzfeldt-Jakob Syndrome and PRNP in his study of Fatal familial insomnia. His Biochemistry study frequently links to related topics such as Oligomer. His Cell biology study integrates concerns from other disciplines, such as Apoptosis, Huntingtin, Hsp70 and Amyloid beta.
Pathology, Biochemistry, Biophysics, Disease and Internal medicine are his primary areas of study. Many of his studies on Pathology apply to IDH1 as well. His Biochemistry study combines topics in areas such as Neurodegeneration, Oligomer and Amyloid.
In his study, Cell biology is inextricably linked to Alpha-synuclein, which falls within the broad field of Biophysics. His Disease research is multidisciplinary, relying on both Phenotype and Genotype. His study in In vitro is interdisciplinary in nature, drawing from both Scrapie, In vivo and Protein folding.
His scientific interests lie mostly in Disease, Biophysics, Internal medicine, Progressive supranuclear palsy and Alpha-synuclein. His Disease research is classified as research in Pathology. His work on Neurodegeneration, Atrophy and Etiology as part of general Pathology study is frequently connected to Herpesviral encephalitis, therefore bridging the gap between diverse disciplines of science and establishing a new relationship between them.
His work in the fields of Biophysics, such as Fibril, overlaps with other areas such as Pore complex. Armin Giese interconnects Endocrinology and Oncology in the investigation of issues within Internal medicine. Many of his research projects under Progressive supranuclear palsy are closely connected to Movement with Movement, tying the diverse disciplines of science together.
The scientist’s investigation covers issues in Progressive supranuclear palsy, Biophysics, Atrophy, Disease and Neuroscience. The various areas that Armin Giese examines in his Progressive supranuclear palsy study include Frontotemporal lobar degeneration, Therapeutic trial and Physical medicine and rehabilitation. His biological study spans a wide range of topics, including Wild type, Cardiolipin and Inner mitochondrial membrane.
His Atrophy research incorporates themes from Randomized controlled trial, Pediatrics and Diagnostic biomarker. Disease is a subfield of Pathology that Armin Giese investigates. In the subject of general Neuroscience, his work in Tyrosine hydroxylase, Cerebellum, Striatum and Pars compacta is often linked to Subthalamic nucleus, thereby combining diverse domains of study.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
The cellular prion protein binds copper in vivo
D R Brown;K Qin;J W Herms;A Madlung.
Nature (1997)
Classification of sporadic Creutzfeldt‐Jakob disease based on molecular and phenotypic analysis of 300 subjects
Piero Parchi;Armin Giese;Sabina Capellari;Paul Brown.
Annals of Neurology (1999)
Different Species of α-Synuclein Oligomers Induce Calcium Influx and Seeding
Karin M. Danzer;Dorothea Haasen;Anne R. Karow;Simon Moussaud.
The Journal of Neuroscience (2007)
Clinical diagnosis of progressive supranuclear palsy: The movement disorder society criteria
Günter U Höglinger;Gesine Respondek;Maria Stamelou;Carolin Kurz.
Movement Disorders (2017)
Prevalence of Superficial Siderosis in Patients with Cerebral Amyloid Angiopathy
J. Linn;A. Halpin;P. Demaerel;J. Ruhland.
Neurology (2010)
Inhibition of mitochondrial fusion by α-synuclein is rescued by PINK1, Parkin and DJ-1.
Frits Kamp;Frits Kamp;Nicole Exner;Nicole Exner;Anne Kathrin Lutz;Nora Wender.
The EMBO Journal (2010)
Evidence of presynaptic location and function of the prion protein.
Jochen Herms;Tobias Tings;Stefan Gall;Axel Madlung.
The Journal of Neuroscience (1999)
Ultrasensitive detection of pathological prion protein aggregates by dual-color scanning for intensely fluorescent targets
J. Bieschke;A. Giese;W. Schulz-Schaeffer;I. Zerr.
Proceedings of the National Academy of Sciences of the United States of America (2000)
Chaperonin TRiC Promotes the Assembly of polyQ Expansion Proteins into Nontoxic Oligomers
Christian Behrends;Carola A. Langer;Raina Boteva;Ulrike M. Böttcher.
Molecular Cell (2006)
Typing prion isoforms
P. Parchi;S. Capellari;S. G. Chen;R. B. Petersen.
Nature (1997)
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