Alzheimer's disease research and treatments

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 identifies two distinct amyloid-β intermediates that drive Alzheimer's pathology and shows their suppression reduces plaque burden and improves cognition in mice.

This study shows fluid amyloid-β biomarkers in 5XFAD mice correlate with β-sheet-rich Aβ deposition during preclinical Alzheimer's disease, with sex differences observed.

The paper analyzes cryo-EM data of CTE tau filaments, identifying a new CTE Type I-like structure with a shifted protofilament interface and showing its coexistence with the canonical CTE Type I structure within fibrils.

This study shows that nuclear acetyl-CoA accumulation in Alzheimer's disease neurons causes RBP hyperacetylation and splicing shifts, which can be reversed by inhibiting ACLY.

The paper links entorhinal cortex-tentorial proximity to tau burden and dementia progression using multimodal imaging data from ADNI.

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 paper models endosomal pH dysregulation in Alzheimer's disease, showing how NHE6 loss leads to hyperacidification, maladaptive plasticity, and Aβ oligomerization.

This study shows that cofilin overexpression suppresses tau- and Aβ-induced defects in dense-core granule formation and neurodegeneration in Drosophila.

This study examines how APOE4, age, and sex affect neuronal properties in the mouse anterior olfactory nucleus through structural and functional analyses.

This study shows that reduced microtubule polyglutamylation causes neuronal dysfunction and worsens Tau-induced neurodegeneration in mice.

This study profiles proteomic changes in iPSC-derived neurons exposed to Aβ42A, revealing AD-related pathways and validating findings in postmortem AD brain tissue.

In a minimal tau fibril model, residue 300/301 binds incoming peptide first and carries the most release-prone hydration water. Spin-labelling site 300 impairs locking and suppresses seeded growth.

This study shows that long-term voluntary exercise in 5xFAD mice leads to limited molecular changes in the hippocampus that do not translate into significant neuroprotection.

This study shows that charge-driven conformational changes in Tau affect its phase behaviour and aggregation propensity.

This study quantifies how α-Synuclein monomers and seeds affect the material properties of Tau condensates, showing distinct effects on viscosity and interfacial tension.

The paper identifies axonal branch points of parvalbumin interneurons as focal sites of Tau-induced degeneration in both mouse and human tauopathy.

This study integrates multiomic data to identify cell-type-specific pathways and therapeutic targets in early Alzheimer's disease.

The paper develops a biophysically realistic model of tau progression that integrates exosome-mediated transport and microtubule dynamics to simulate macroscopic spread in the brain.

The paper uses MALDI-TOF imaging to show sex- and age-dependent changes in brain metabolites and histone lactylation in a mouse Alzheimer's model, linking them to metabolic-epigenetic coupling and sex-specific AD vulnerability.

This study shows that GDE2 modulates Tau phosphorylation in a region-specific manner in a mouse tauopathy model, affecting kinase activity and Tau aggregation propensity.

The paper constructs a lifespan single-cell atlas of the human developing hippocampus and benchmarks iPSC-derived brain organoids with a PSEN1 mutation linked to familial Alzheimer's disease.

The paper estimates heritability and identifies genetic variants, including rare ones, associated with Alzheimer disease in the Amish population.

This study shows that Rab11-exosome biogenesis regulators like Chmp5 control Aβ-induced endolysosomal trafficking defects and neurodegeneration in Drosophila.

The paper investigates off-target interactions of amyloid PET tracers with brain sulfotransferases using multi-omic and computational methods, revealing enzyme-specific binding dynamics and implications for PET signal variability.

This study shows how neuronal lipid composition affects full-length tau assembly, mechanics, and membrane interactions, revealing distinct states of tau-membrane interaction based on lipid type and tau assembly state.

The paper identifies a helix-loop-helix motif in ApoE3 that binds TREM2 using XL-MS and de novo protein design.

This study shows that impaired glutathione (GSH) and β-amyloid (Aβ) synergistically drive lipid peroxidation and ferroptosis in neuron-like cells, highlighting redox dysregulation as a key factor in Alzheimer's disease.

This study shows that mTOR inhibition restores RNA-regulatory proteins in AD models, suggesting a reversible mTOR-dependent RNA regulatory program in cerebrovascular dysfunction.