Nobutaka Hattori

The paper uses salivary microbiome profiles to stratify REM sleep behavior disorder and synucleinopathies, finding distinct microbial signatures that distinguish these conditions.

The paper reports the structures of α-synuclein filaments from individuals with Parkinson's disease and dementia, revealing differences in dimerisation and twist reversal between pathogenic and non-pathogenic variants.

This study identifies tegmental atrophy in iRBD using VBM and a novel brainstem atlas, linking atrophy in specific nuclei to autonomic dysfunction.

This study identifies genetic associations between lysosomal genes and Parkinson's disease risk across diverse populations using GWAS and whole genome sequencing data.

The paper identifies the LRRK2 p.A419V variant as a significant risk factor for Parkinson's disease in East Asian populations and explores its association with age of onset.

This study compares long-read sequencing and optical genome mapping in detecting structural variants in Parkinson's disease, finding OGM better detects large variants while ONT provides high-resolution refinement.

This paper investigates the role of alpha-synuclein in lipid regulation at MAM domains in synucleinopathies, showing disease-specific lipid alterations and Syn's impact on phosphatidylserine metabolism.

This study examines PINK1-PRKN signaling in mice during aging, showing increased gene expression and enzymatic activity in multiple tissues, with the heart showing the most pronounced activation.

This study identifies four cell types in the mouse PVT using single-cell RNA sequencing and shows their transcriptomic continuity along the anterior-posterior axis, with distinct axon projection patterns and functional responses to neuropeptides.

The paper identifies mitochondrial DNA heteroplasmy as a marker distinguishing disease manifestation in PINK1/PRKN mutation carriers.

This study shows that high-fat diet-induced activation of SGK1 promotes tau pathology in Alzheimer's disease by phosphorylating tau and activating GSK-3β.

This study investigates how parkin's redox state and insolubility in human midbrain relate to oxidative stress and dopamine metabolism, showing that parkin's cysteine modifications affect H2O2 levels and neuroprotection.

This study shows that parkin reduces oxidative stress in mammalian brains by mediating H2O2 reduction and glutathione regeneration, but its absence leads to increased oxidative stress despite compensatory mechanisms.

This study identifies oxidative modifications of parkin in adult human brain that confer neuroprotection by reducing H2O2, conjugating dopamine radicals, and forming neuromelanin.