Cytosolic aggregation of mitochondrial proteins disrupts cellular homeostasis by stimulating the aggregation of other proteins.

Exogenous misfolded protein oligomers can cross the intestinal barrier and cause a disease phenotype in C. elegans.

Two human metabolites rescue a C. elegans model of Alzheimer's disease via a cytosolic unfolded protein response.

Squalamine and Its Derivatives Modulate the Aggregation of Amyloid-β and ι-Synuclein and Suppress the Toxicity of Their Oligomers.

Parallel and Sequential Pathways of Molecular Recognition of a Tandem-Repeat Protein and Its Intrinsically Disordered Binding Partner.

Scaling analysis reveals the mechanism and rates of prion replication in vivo.

Characterisation of the structural, dynamic and aggregation properties of the W64R amyloidogenic variant of human lysozyme.

The release of toxic oligomers from Îą-synuclein fibrils induces dysfunction in neuronal cells.

Comparative Studies in the A30P and A53T Îą-Synuclein C. elegans Strains to Investigate the Molecular Origins of Parkinson's Disease.

Aβ Oligomers Dysregulate Calcium Homeostasis by Mechanosensitive Activation of AMPA and NMDA Receptors.

Publisher Correction: A dopamine metabolite stabilizes neurotoxic amyloid-β oligomers.

Systematic Activity Maturation of a Single-Domain Antibody with Non-canonical Amino Acids through Chemical Mutagenesis.

A dopamine metabolite stabilizes neurotoxic amyloid-β oligomers.

Screening of small molecules using the inhibition of oligomer formation in Îą-synuclein aggregation as a selection parameter.

Kinetic fingerprints differentiate the mechanisms of action of anti-Aβ antibodies.