Emre Fertan

The paper shows TNFα promotes tau aggregation at pre-synapses in human neurons, forming non-fibrillar aggregates that replicate rapidly.

The paper identifies disease-specific molecular profiles of small tau aggregates across different tauopathies using single-molecule assays.

The paper examines tau aggregates in Alzheimer's disease synaptosomes, finding that small tau aggregates are associated with early synaptic pathology.

The paper uses super-resolution microscopy and SIMOA to analyze alpha-synuclein aggregates in Parkinson's disease brain samples and mouse models, finding larger aggregates in PD samples and differences based on extraction methods.

The paper identifies a cellular tipping point between aggregate accumulation and removal as a universal feature of neurodegeneration, validated through live-cell assays and super-resolution imaging.

This study shows human astrocytes generate and release amyloid-β aggregates under lysosomal stress, contributing to extracellular Aβ accumulation in Alzheimer's disease.

The paper uses single-molecule detection and super-resolution imaging to analyze how four monoclonal antibodies bind to beta-amyloid aggregates, finding Lecanemab has superior binding properties.

SynPull combines single-molecule pulldown, super-resolution microscopy, and computational analysis to study protein aggregates in synaptosomes from human and mouse samples, revealing AT8-positive tau as the predominant aggregate in Alzheimer's disease.

This study shows that oligodendrocytes produce amyloid beta in Alzheimer's Disease and that suppressing this production improves brain pathology and neuronal function.