Alzheimer's disease research and treatments

This study uses NMR-pharmacometabolomics to investigate how nicotine mitigates amyloid toxicity in SH-SY5Y cells, revealing its role in restoring metabolic imbalances linked to Alzheimer's disease.

This study investigates the cell-specific transcriptional responses to bexarotene in Alzheimer's disease mouse models, revealing APOE's role in RXR-mediated neuroprotection.

This study evaluates a natural compound (MIC) that reduces tau pathology and microglial reactivity in 3xTgAD mice and rescues working memory, suggesting it as a potential therapeutic for Alzheimer's disease.

The paper identifies early vascular remodeling features in Alzheimer's disease using cross-species analysis linking mouse and human data.

The paper investigates how tau's liquid-liquid phase separation affects its binding to BRICHOS and tubulin, showing conformational changes regulate these interactions.

This paper introduces a mouse model for Alzheimer's disease that allows testing of human cell therapies without immune rejection.

This study shows genetic liability to hip osteoarthritis protects against Alzheimer's disease through neurovascular mechanisms, but this protection is masked by depression-related comorbidity.

This study shows tubulin modulates Tau and synuclein condensates from pathological to physiological by promoting microtubule interactions and preventing aggregation.

The paper identifies epigenetic changes in Alzheimer's disease brains linked to tau pathology, highlighting oligodendrocyte gene perturbations as a potential common mechanism across tauopathies.

The paper confirms non-neuronal Tau expression in multiple tissues of humans and mice using validated antibodies and tissue microarrays.

This study shows that removing visceral adipose tissue in male APPNL-F mice improves metabolism and cognition, while females show different metabolic responses and no cognitive benefit.

This study investigates the effect of orexin receptor antagonists on early-stage Alzheimer's disease in mice, finding they prevent cognitive impairment and amyloid-beta accumulation.

This study identifies Dgat2 as a key modulator linking amyloid pathology, lipid dysregulation, and neuroinflammation in Alzheimer's disease across Drosophila and mouse models.

This study compares [125I]IPPI and [125I]IBETA binding in brain tissues of AD, DSAD, and CN to assess their potential as radiotracers for tau and Aβ plaques.

This study shows that cDC1 cells prime CD8+ T cells, which then exacerbate tau-mediated neurodegeneration in mice.

This study identifies Hopx as a regulator of astrocytic function in Alzheimer's disease, showing that its expression is linked to Aβ clearance and reduced neurotoxic astrocyte generation.

This study shows APOE3 astrocytes rescue lipid-induced neurite damage in APOE4 neurons by enhancing lipid homeostasis through HDL-like particle production.

This paper uses membrane-mimetic proteomics to show that AD-related membrane proteome changes are enriched in APP mice, and M1 receptor activation selectively affects disease-altered membrane networks.

This study shows that elevating neuronal CYLD causes FTD-like behavioral and physiological deficits in mice, with M719V mutation acting as a gain-of-function.

This study examines how different amyloid-beta fibrils affect sleep and cortical activity in mice, revealing distinct impacts of Aβ40 and Aβ42.

This study investigates how JHMV-induced encephalitis affects Aβ plaque pathology in 5xFAD mice, finding increased T cell infiltration and altered myeloid cell responses.

This study shows that human tau and amyloid-β pathology alter tau propagation patterns and cause neurophysiological dysfunction in mouse models of tauopathy and Alzheimer's disease.

This study identifies two epigenomic subtypes of late-onset Alzheimer's disease with distinct microglial and neuronal methylation signatures, linking them to different inflammatory and functional pathways.

This study shows that miR-34a deficiency in Alzheimer's disease mice increases type I IFN signaling and microglial activation, linked to improved memory and altered amyloid-beta ratios.

The paper shows that Aβ and mutant Tau reduce neuronal activity in young C. elegans before amyloid aggregation, with muscle-expressed Aβ affecting neurons via retrograde signaling.

This study shows that p75NTR signaling through the RhoA/ROCK pathway contributes to Alzheimer's Disease tauopathy, with specific receptor variants reducing neurodegeneration and cognitive impairment.

The paper uses isogenic cortical organoids to identify variant-specific pathogenic pathways in Alzheimer's disease and demonstrates targeted interventions that restore neuronal survival.

This study shows that tau propagation from entorhinal cortex to hippocampal CA1 neurons leads to sex-specific cognitive and electrophysiological impairments, driven by distinct neuroimmune responses in males and females.

This study identifies two distinct binding modes for high-affinity ligand interactions with amyloid fibrils and demonstrates how these modes can inform ligand design improvements.