Johannes Burtscher

Development and validation of an expanded antibody toolset that captures alpha-synuclein pathological diversity in Lewy body diseases

The paper develops and validates an expanded antibody panel to capture diverse alpha-synuclein conformations and modifications in Lewy body diseases.

Post-fibrillization nitration of alpha-synuclein abolishes its seeding activity and pathology formation in primary neurons and in vivo

This study shows that nitration of alpha-synuclein after fibrillization reduces its seeding activity and pathology formation in neurons and in vivo.

Nuclear and cytoplasmic huntingtin inclusions exhibit distinct biochemical composition, interactome and ultrastructural properties

The paper examines the biochemical composition, interactome, and ultrastructural properties of nuclear and cytoplasmic Htt inclusions in mammalian cells and neurons.

Pronounced α-synuclein pathology in a seeding-based mouse model is not sufficient to induce mitochondrial respiration deficits in the striatum and amygdala

This study shows that early α-synuclein pathology in a mouse model does not cause mitochondrial respiration deficits in the striatum and amygdala, even under corticosterone-induced hyperactivity.

The process of Lewy body formation, rather than simply alpha-synuclein fibrillization, is the major driver of neurodegeneration in synucleinopathies

This study develops a neuronal model of Lewy body formation and shows that the process of Lewy body maturation, not just fibrillization, drives neurodegeneration in synucleinopathies.

The making of a Lewy body: the role of alpha-synuclein post-fibrillization modifications in regulating the formation and the maturation of pathological inclusions.

Calpain-1/2 cleavage of the alpha-synuclein C-terminus after fibril formation is reported to drive seeding, aggregation and the maturation of Lewy-body-like inclusions in primary neurons.

Chronic corticosterone enhancement aggravates alpha-synuclein brain spreading pathology and substantia nigra neurodegeneration in mice

This study shows that chronic corticosterone worsens alpha-synuclein pathology and neurodegeneration in a mouse model of Parkinson's disease.