Charles L. White

Large-Scale Mutagenesis Identifies Sequence Changes That Bias Tau Toward CTE-like Aggregation

The paper identifies sequence changes that bias tau aggregation toward CTE-like structures using mutagenesis and structural analysis.

Targeted single-nucleus sequencing of 39,800 neurons reveals extensive low-frequency somatic variants

The paper analyzes somatic mutations in neurons from FTLD-TDP type C patients and controls, finding extensive low-frequency variants in TARDBP and other genes.

TAF15 amyloids propagate via defined motifs in a prion-like fashion

This study shows TAF15 forms amyloid fibrils and propagates prion-like between cells, identifying specific motifs that drive its aggregation in vitro and in cells.

Cysteines are critical determinants of spontaneous and seeded tau aggregation in cells

This study identifies cysteine residues as critical for tau aggregation and propagation in cells, both spontaneously and when seeded.

Deciphering Distinct Genetic Risk Factors for FTLD-TDP Pathological Subtypes via Whole-Genome Sequencing

This study identifies genetic risk factors for FTLD-TDP subtypes using whole-genome sequencing and meta-analysis across multiple cohorts.

Functional classification of tauopathy strains reveals the role of protofilament core residues.

The paper identifies amino acids critical for tau strain propagation by analyzing their role in amyloid templating across different tauopathies.

Selective Targeting of Pathogenic Tau Seeds via a Novel VHH

This paper identifies two VHH antibodies that selectively bind pathogenic tau seeds in AD and related tauopathies, showing potential for therapeutic and diagnostic applications.

Essential tremor with tau pathology features seeds indistinguishable in conformation from Alzheimer's disease and primary age-related tauopathy

This study identifies that tau assemblies in a subset of essential tremor cases with tau pathology are conformationally similar to Alzheimer's disease and primary age-related tauopathy.

Whole-Genome Sequencing Analysis Reveals New Susceptibility Loci and Structural Variants Associated with Progressive Supranuclear Palsy

This study uses whole-genome sequencing to identify new genetic loci and structural variants associated with progressive supranuclear palsy, including novel signals in APOE and H1/H2 haplotype region variants.

Tau seeding without tauopathy

The paper detects seeding activity of tau assemblies in healthy human brains, suggesting normal physiological tau function that may contribute to disease when disrupted.

Anti-tau antibodies targeting a conformation-dependent epitope selectively bind seeds

The paper develops anti-tau antibodies that selectively bind pathological tau seeds in neurodegenerative diseases, supporting a model of conformational change at P301.

DnaJC7 specifically regulates tau seeding

This study identifies DnaJC7 as a specific regulator of tau seeding through its interaction with Hsp70, showing that its protective activity depends on the J domain and substrate binding site.

Network of hotspot interactions cluster tau amyloid folds

The paper uses an in silico alanine scan method to identify energetically important interactions in tau amyloid fibrils and classifies structures using machine learning.

Genome-wide association study of autopsy-confirmed Multiple System Atrophy identifies common variants near ZIC1 and ZIC4

Seed-competent tau monomer initiates pathology in PS19 tauopathy mice

The paper shows that seed-competent tau monomer (Ms) forms before insoluble fibrils in PS19 tauopathy mice, initiating pathology in a phosphorylation-independent manner.

Genome-wide association study and functional validation implicates JADE1 in tauopathy

This study identifies JADE1 as a novel genetic factor in tauopathy through genome-wide association and functional validation in human and Drosophila models.

NHE6-Depletion Corrects ApoE4-Mediated Synaptic Impairments and Reduces Amyloid Plaque Load

This study shows that NHE6 inhibition corrects ApoE4-mediated synaptic impairments and reduces amyloid plaque load, suggesting a potential therapeutic strategy for Alzheimer's disease.