Carsten Korth

Abbreviated incubation times for human prions in mice expressing a chimeric mouse-human prion protein transgene.

The expanded octarepeat domain selectively binds prions and disrupts homomeric prion protein interactions.

Prion protein gene codon 129 modulates clinical course of neurological Wilson disease.

Emerging pharmacotherapies for Creutzfeldt-Jakob disease.

Tricyclic antidepressants, quinacrine and a novel, synthetic chimera thereof clear prions by destabilizing detergent-resistant membrane compartments.

Similar structure-activity relationships of quinoline derivatives for antiprion and antimalarial effects.

A chimeric ligand approach leading to potent antiprion active acridine derivatives: design, synthesis, and biological investigations.

The use of conformation-specific ligands and assays to dissect the molecular mechanisms of neurodegenerative diseases.

Vaccine approaches to prevent and treat prion infection : progress and challenges.

Insolubility of disrupted-in-schizophrenia 1 disrupts oligomer-dependent interactions with nuclear distribution element 1 and is associated with sporadic mental disease.

Expansion of the octarepeat domain alters the misfolding pathway but not the folding pathway of the prion protein.

Genes contributing to prion pathogenesis.

Complementarity determining regions of an anti-prion protein scFv fragment orchestrate conformation specificity and antiprion activity.

Quinpramine 是一个新型的复合有效改善大脑自身免疫性疾病。

Genetic polymorphism at codon 129 of the prion protein gene is not associated with multiple sclerosis.

Oligomer assembly of the C-terminal DISC1 domain (640-854) is controlled by self-association motifs and disease-associated polymorphism S704C.

Binding of TCA to the prion protein: mechanism, implication for therapy, and application as probe for complex formation of bio-macromolecules.

alpha-secretase mediated conversion of the amyloid precursor protein derived membrane stub C99 to C83 limits Abeta generation.

Understanding the role of DISC1 in psychiatric disease and during normal development.

Structure-activity relationship of tocopherol derivatives suggesting a novel non-antioxidant mechanism in antiprion potency.

Microdeletions within the hydrophobic core region of cellular prion protein alter its topology and metabolism.

Pharmacological prion protein silencing accelerates central nervous system autoimmune disease via T cell receptor signalling.

Disrupted-in-Schizophrenia-1 expression is regulated by beta-site amyloid precursor protein cleaving enzyme-1-neuregulin cascade.

DISCopathies: brain disorders related to DISC1 dysfunction.

Codon 129 polymorphism and the E200K mutation do not affect the cellular prion protein isoform composition in the cerebrospinal fluid from patients with Creutzfeldt-Jakob disease.

Quinpramine--a promising compound for treating immune-mediated demyelination of the nervous system.

Human prion strain selection in transgenic mice.

Combining independent drug classes into superior, synergistically acting hybrid molecules.

Presenilin-1 but not amyloid precursor protein mutations present in mouse models of Alzheimer's disease attenuate the response of cultured cells to γ-secretase modulators regardless of their potency and structure.

No association between genetic polymorphism at codon 129 of the prion protein gene and primary progressive multiple sclerosis.

Biological effects and use of PrPSc- and PrP-specific antibodies generated by immunization with purified full-length native mouse prions.

Convergence of two independent mental disease genes on the protein level: recruitment of dysbindin to cell-invasive disrupted-in-schizophrenia 1 aggresomes.

Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules.

Rapidly progressive Alzheimer disease.

Hybrid compounds: from simple combinations to nanomachines.

Cellular prion protein participates in amyloid-β transcytosis across the blood-brain barrier.

Aggregated proteins in schizophrenia and other chronic mental diseases: DISC1opathies.

Identification of I137M and other mutations that modulate incubation periods for two human prion strains.

C-terminal fragment of N-cadherin accelerates synapse destabilization by amyloid-β.

Human and rat brain lipofuscin proteome.

Identification of Dominant Human Aquaporin 4 T-Cell Epitopes: Observations in Neuromyelitis Optica With Implications for Other Autoimmune DisordershAQP4 T-Cell Epitopes.

Oral Treatment with the d-Enantiomeric Peptide D3 Improves the Pathology and Behavior of Alzheimer's Disease Transgenic Mice.

Molecular engineering of a secreted, highly homogeneous, and neurotoxic aβ dimer.

Proteomic, genomic and translational approaches identify CRMP1 for a role in schizophrenia and its underlying traits.

On the issue of transmissibility of Alzheimer disease: a critical review.

Characterization of a single-chain variable fragment recognizing a linear epitope of aβ: a biotechnical tool for studies on Alzheimer's disease?

Immunohistochemical characterization of novel monoclonal antibodies against the N-terminus of amyloid β-peptide.

Revisiting Disrupted in Schizophrenia 1 as a scaffold protein.

Regulation of N-Methyl-D-Aspartate Receptors by Disrupted-in-Schizophrenia-1.