Masato Hasegawa

This study demonstrates that tau filaments from Alzheimer's and corticobasal degeneration patients can seed the formation of structurally identical mouse tau filaments, supporting the prion-like transmission hypothesis.

This study shows that α-synuclein aggregates cause mitochondrial damage and activate innate immunity, leading to neuron-microglia communication via TNTs and promoting disease progression in Synucleinopathies.

The paper shows that neuronal autophagy failure leads to α-synuclein aggregate transfer to microglia, which then degrade them more efficiently.

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 develops a PET ligand to visualize α-synuclein pathologies in Parkinson's and DLB patients, showing increased signals in affected brain regions.

The paper reports that tau filaments in vacuolar tauopathy with VCP mutation D395G have the CTE fold, similar to environmentally induced diseases.

The paper reports cryo-EM structures of tau filaments formed in SH-SY5Y cells seeded with brain extracts from Alzheimer's and corticobasal degeneration cases, showing some structural templating.

This study shows that tau filaments in subacute sclerosing panencephalitis and chronic traumatic encephalopathy have identical structural features.

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

The paper reports cryo-EM structures of α-synuclein filaments from Parkinson's disease, PD dementia, and dementia with Lewy bodies, showing they are composed of a single protofilament distinct from those in multiple system atrophy.

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 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.

This study identifies plexin-B3+ oligodendrocyte precursor cells as potential amyloid beta-secreting cells in Alzheimer's disease.

This paper develops a peptide inhibitor, RI-AG03, that reduces Tau aggregation in vitro and improves Tauopathy symptoms in Drosophila.

The paper shows that different α-synuclein strains cause distinct pathologies by differentially inhibiting proteasome activity through structural differences in their C-terminal regions.

This study determines the structure of α-synuclein filaments in multiple system atrophy using cryo-EM, revealing distinct filament types and conformers that differ from in vitro assemblies.

This study shows that early-life stress accelerates Alzheimer's disease pathology by inducing vascular changes and microglia activation in mice with an APP mutation.

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