Area of research
Physiology · Biophysics
Research interest
Research interests include Chemistry, Biophysics, Cell biology, Biology, Alpha-synuclein, and Intracellular.
Lecanemab preferentially binds to smaller aggregates present at early Alzheimer's disease
Detection of p53 aggregates in plasma of glioma patients
Quantitative Profiling of Nanoscopic Protein Aggregates Reveals Specific Fingerprint of TDP‐43‐Positive Assemblies in Motor Neuron Disease
APOE from astrocytes restores Alzheimer’s Aβ-pathology and DAM-like responses in APOE deficient microglia
Single-molecule characterization of salivary protein aggregates from Parkinson’s disease patients: a pilot study
Characterization of full-length p53 aggregates and their kinetics of formation
Single-molecule visualization of DNA G-quadruplex formation in live cells
Alpha synuclein aggregation drives ferroptosis: an interplay of iron, calcium and lipid peroxidation
Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death
ThX – a next-generation probe for the early detection of amyloid aggregates
Insoluble tau aggregates induce neuronal death through modification of membrane ion conductance, activation of voltage‐gated calcium channels and NADPH oxidase
α-Synuclein strains target distinct brain regions and cell types
Secondary nucleation and elongation occur at different sites on Alzheimer’s amyloid-β aggregates
ThX – A next-generation probe for the early detection of amyloid aggregates
FUS Phase Separation Is Modulated by a Molecular Chaperone and Methylation of Arginine Cation-π Interactions
α-synuclein oligomers interact with ATP synthase and open the permeability transition pore in Parkinson’s disease
The small heat shock protein Hsp27 binds α-synuclein fibrils, preventing elongation and cytotoxicity
Activation of Toll-like receptors nucleates assembly of the MyDDosome signaling hub
Single-Molecule Characterization of the Interactions between Extracellular Chaperones and Toxic α-Synuclein Oligomers
Ca2+ is a key factor in α-synuclein-induced neurotoxicity
Arachidonic acid mediates the formation of abundant alpha-helical multimers of alpha-synuclein
Rare Individual Amyloid-β Oligomers Act on Astrocytes to Initiate Neuronal Damage
Single Molecule Characterization of the Interactions between Amyloid-β Peptides and the Membranes of Hippocampal Cells
Amyloid-β Oligomers are Sequestered by both Intracellular and Extracellular Chaperones