Alzheimer's disease research and treatments

Brain single-cell transcriptional responses to bexarotene-activated RXR in Alzheimer's disease model

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

A Compound Enhancing Lysosomal Function Reduces Tau Pathology, Microglial Reactivity and Rescues Working Memory in 3xTg AD Mice

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.

Linking cross-species trajectories of cerebrovascular remodeling in aging and Alzheimer's disease to brain vessel transcriptome

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

Liquid-liquid phase separation of tau regulates client binding via a conformational relay

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

5xFAD-NSG mice: a preclinical Alzheimer model for human cell therapy studies

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

Genetic liability to hip osteoarthritis confers neurovascular protection against Alzheimer's disease despite depression-mediated phenotypic comorbidity

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.

Tubulin transforms Tau and -synuclein condensates from pathological to physiological

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

Integrative Epigenomic Landscape of Alzheimer's Disease Brains Reveals Oligodendrocyte Molecular Perturbations Associated with Tau

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.

Expression of non-neuronal Tau in humans and mice

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

Surgical Removal of Visceral Adipose Tissue has Therapeutic Benefit in Male APPNL-F Mice

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.

Involvement of orexin nerves in early stage of Alzheimer's disease model mice and preventive effect of orexin receptor antagonists

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.

Regulation of lipid dysmetabolism and neuroinflammation progression linked with Alzheimer's disease through modulation of Dgat2

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

Measurement of tau protein and Aβ amyloid plaques in postmortem human brains of Down syndrome and Alzheimers disease by using IBETA autoradiography

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.

CD8+ T cells are primed by cDC1 and exacerbate tau-mediated neurodegeneration

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

Hopx expression marks Aβ clearance astrocytes in Alzheimers disease

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.

APOE3 astrocytes can rescue lipid abnormalities and dystrophic neurites of APOE4 human neurons

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

The microtubule nexus linking amyloid beta and tau: A simple and unifying theory for the underlying cause of Alzheimer's Disease

Membrane Proteome Remodeling in Female APP Mice Following Muscarinic Acetylcholine Receptor M1 Modulation Revealed by Peptidisc Enabled DIA-MS.

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.

Elevating Neuronal CYLD Causes Frontotemporal Dementia (FTD)-Relevant Behavioral and Physiological Deficits

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.

Amyloid fibrils in Alzheimer's disease differently modulate sleep and cortical oscillations in mice depending on the type of amyloid

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

Characterization of effects of a neurotropic murine coronavirus infection on Alzheimer's disease neuropathology of 5xFAD mice

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

Humanized tau and amyloid-β deposition accelerate tau propagation, neuronal cell loss and neurophysiological dysfunction in novel mouse models of primary age-related tauopathy and Alzheimer's disease

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.

Epigenomic subtypes of late-onset Alzheimer's disease reveal distinct microglial signatures

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.

MiR-34a deficiency enhances nucleic acid sensing and type I IFN signaling in a mouse model of Alzheimer's disease

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.

Impairment of neuronal activity occurs at the early stages of the aggregation cascade of Ab1-42 and mutant Tau

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.

p75 neurotrophin receptor signaling through the RhoA/ROCK pathway contributes to Alzheimers Disease tauopathy

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.

Isogenic cortical organoids enable precision targeting of APP variant-specific pathways in Alzheimer's disease

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

Entorhinal Cortex Wolframin-1-expressing neurons propagate tau to CA1 neurons and impair hippocampal memory

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.

Two Distinct Binding Modes Govern High-Affinity Ligand Interactions with Amyloid Fibrils

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.

Structural defects in amyloid-β fibrils drive secondary nucleation

This study shows that structural defects in amyloid-β fibrils are key sites for secondary nucleation, suggesting new strategies for drug design to inhibit amyloid disorders.