Benjamin L. Wolozin

The paper maps protein interaction network remodeling in a mouse tauopathy model using multi-omics and machine learning, identifying key complexes involved in early disease phenotypes.

This study shows that loss of normal Tau function in the adult brain causes neuronal atrophy, epigenetic changes, and cognitive/mood deficits, which can be reversed by Tau re-expression or epigenetic correction.

The paper develops nanobodies targeting hnRNPA2/B1 and tau, showing they colocalize with targets and can reduce protein levels when fused to ubiquitin ligase domains.

This study investigates age- and pathology-dependent changes in the epitranscriptome and translational dysfunction in a tauopathy mouse model, revealing significant alterations in tRNA biology and codon usage patterns.

The paper shows that loss of age-related m6A RNA methylation in Alzheimer's disease brains is linked to GABAergic dysfunction and synaptic issues.

This study shows GSK3β phosphorylation drives tau aggregation into Alzheimer's-like amyloid strains through enhanced phase separation.

This study shows TIA1 regulates divergent inflammatory responses in microglia and macrophages, reducing brain inflammation and tau pathology while increasing peripheral inflammation.

This study identifies differentially expressed genes and pathways in Alzheimer's disease brain tissue from African American donors, highlighting potential targets for treatment.

The paper uses proximity labeling to study the dynamic SQSTM1 protein network and shows that aggregated tau alters its interactions with stress-associated proteins.

The paper shows that ORF57 from Human Herpesvirus 8 reduces TDP-43 aggregation and cell death by interacting with ISR components.

This study shows that m6A accumulation correlates more strongly with MAPT pathology than beta-amyloid in an Alzheimer's mouse model.

The paper identifies circRNAs associated with Alzheimer's disease and related dementias through transcriptome analysis and validates their expression in neuronal precursor cells exposed to oligomeric tau.

The paper develops a 3D neuron-astrocyte coculture model to study tauopathy, showing it recapitulates pathological features and responds to HSP90 inhibitor treatment.

The paper identifies a dynamic hnRNP H RNA targetome in the striatum that responds to methamphetamine, affecting gene expression and behavior.

The paper shows that ApoE alleles compete with mCRP for CD31 binding on brain endothelia, leading to differential AD pathology based on ApoE genotype.

This paper identifies a complex involving HNRNPA2B1, N6-methyladenosine modified transcripts, and toxic tau oligomers that mediates neurodegeneration.

The paper identifies 5' UTR variants in Hnrnph1 that reduce 5' UTR usage and hnRNP H protein levels, linking these changes to reduced methamphetamine sensitivity.

This study identifies a mutation in Hnrnph1 that reduces methamphetamine-induced reinforcement, reward, and dopamine release while increasing synaptic hnRNP H and mitochondrial proteins in mice.

The paper examines changes in hnRNP H localization in primary rat cortical neurons after D1 dopamine receptor activation, finding increased nuclear immunostaining of the C-terminal domain without changes in protein levels.