Benjamin Falcon

This study shows TDP-43 filaments accumulate at synapses, causing presynaptic dysfunction and neuronal hyperexcitability in neurodegenerative diseases.

This study identifies distinct TAF15 amyloid filament structures in different FTLD-FET subtypes, leading to the renaming of the disease group as FTLD-TAF15.

The paper identifies tau filaments within extracellular vesicles from Alzheimer's disease patients using mass spectrometry and cryo-electron microscopy.

This study identifies heteromeric amyloid filaments composed of ANXA11 and TDP-43 in FTLD-TDP Type C using cryo-EM, revealing a new pathological mechanism.

This study uses cryo-EM to show that tau filaments in ALS/PDC share the CTE fold, suggesting environmental causes for the disease.

This study identifies age-dependent formation of TMEM106B amyloid filaments in human brains using cryo-EM, showing they appear in older individuals but not younger ones.

Cryo-EM shows brain-derived Aβ42 filaments adopt two related S-shaped protofilament folds: Type I dominates sporadic Alzheimer's, Type II familial Alzheimer's, other disorders and App^NL-F knock-in mice.

Cryo-EM structures sort four-repeat tauopathies into three-layered (PSP, GGT, LNT) and four-layered (CBD, AGD, ARTAG, MAPT intron 10 mutations) tau folds, grounding a hierarchical structure-based classification.

The paper identifies LRRK2-regulated pathways for extracellular tau uptake in human neurons using CRISPR screens, showing LRRK2's role in monomeric tau endocytosis.

This paper reports the structure of tau filaments in corticobasal degeneration using cryo-EM, revealing a novel four-layered fold distinct from other tauopathies.

The paper determines the structure of tau filaments in Alzheimer's disease cases and finds they adopt a common fold across individuals.