Alzheimer's disease research and treatments

The paper isolates and analyzes amyloid fibrils from AD brains and models to identify proteins associated with fibril formation and toxicity, finding new proteins and validating their roles.

This study investigates how the size and motional dynamics of beta amyloid oligomers relate to their cytotoxicity, finding that smaller oligomers are more toxic due to increased motion of charged residues.

This study identifies the dentate gyrus as the dominant site of interictal spikes in Alzheimer's disease models and shows that cholinergic control from the medial septum modulates these spikes during REM sleep.

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

The paper investigates spatial disorientation and hemispheric neurodegeneration in TgF344-AD rats, finding asymmetrical neurodegeneration and impaired spatial memory.

This study establishes a mechanistic model of amyloid oligomer and protofibril formation in bovine insulin using light scattering and kinetic analysis, revealing end-to-end association as the rate-limiting step.

The paper develops a platform combining yeast and phage display to screen peptide therapeutics for neurodegenerative diseases, identifying candidates that inhibit amyloid fibril formation.

The paper identifies common molecular signatures between coronavirus infection and Alzheimer's disease to suggest potential therapeutic targets.

This study produces stable, on-pathway oligomers of hIAPP using mechanical rotation during MAS NMR, showing sensitivity to sample conditions and potential for studying other aggregating systems.

The paper investigates the impact of elevated cystatin B on cathepsin B activity and microglial localization in Alzheimer's disease in Down syndrome and early-onset Alzheimer's disease.

This study selects conformational nanobodies specific for aggregated tau using flow cytometry, showing their utility in detecting tau aggregates in mouse and human samples.

The paper investigates the association between low circulating choline and Alzheimer's disease progression, finding it linked to neuropathological features and metabolome dysfunction.

The paper compares transcriptomes of excitatory neurons from Alzheimer's patients and controls, identifying 621 differentially expressed genes and linking them to known Alzheimer's genes and functional networks.

The paper investigates dimerization of APP family members in cultured cells and mouse brains, finding higher dimerization in brain tissue and enrichment in synaptic compartments, with reduced dimers in AD patients.

The paper investigates how genetic background affects tau aggregate seeding in mice by analyzing RNA-seq and tau seeding activity data from four strains.

This study identifies that phosphorylated APP βCTF inhibits v-ATPase in Down Syndrome and Alzheimer's models, leading to lysosomal dysfunction.

This study investigates how altering the APP-Mint1 interaction affects amyloid-beta production and cellular dynamics in neurons.

The paper compares proteomic profiles of cerebrospinal fluid from African Americans and Caucasians with and without Alzheimer's disease to identify shared and divergent biomarkers.

This study identifies Arl8b as a potential biomarker for Alzheimer's disease by analyzing proteomic changes in 5xFAD mouse brain regions and CSF from AD patients.

This study examines vascular and metabolic changes in 5xFAD mice over time, finding sex-specific differences in vascular features and glucose metabolism linked to Alzheimer's pathology.

The paper examines transcriptomic changes in Alzheimer's disease brain regions associated with Aβ plaques, tangles, and APOE ε4, finding distinct gene expression patterns linked to neuroinflammation and neuronal dysfunction.

This paper develops a mathematical model to study how brain clearance mechanisms interact with toxic protein progression and aging in neurodegenerative diseases like Alzheimer's.

This paper designs a β-helix tau protein scaffold that mimics toxic tau oligomers and shows selective binding to antibodies, suggesting it could be an effective vaccine immunogen for Alzheimer's disease.

The paper identifies a tau-first subtype of Alzheimer's disease through analysis of post mortem and in vivo data, showing higher soluble TREM2 levels in tau-first cases.

This study shows that lamivudine reduces tauopathy-related pathology and behavioral deficits in P301S mice by inhibiting LINE-1 retrotransposition.

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.

The paper compares the bioactivity of fibrillar and oligomeric tau forms in Alzheimer's disease, finding HMW tau more potent in glial activation and tau propagation.

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.