Alzheimer's disease research and treatments

The paper uses AI to analyze spatial data from Alzheimer's mouse models, revealing new protein interactions and synaptic structures linked to disease.

The paper identifies cell type-specific lipid and protein compositions of apoE lipoproteins secreted by different brain cell types and found in cerebrospinal fluid.

This study identifies cell-type-specific histone acetylation changes in Alzheimer's disease, highlighting MITF's potential role in microglial dysfunction.

The paper investigates how pathological tau affects gene expression in a Drosophila tauopathy model, finding increased RNA polymerase II pausing linked to reduced expression of long neuronal genes.

This study shows that soluble pathogenic tau aggregates are transmitted to astrocytes, causing mitochondrial dysfunction, senescence, and neurovascular uncoupling in a tauopathy model.

The paper models A{beta} dynamics across brain, CSF, and plasma during sleep and wakefulness, showing increased CSF A{beta}42 levels after sleep due to sampling effects and impaired clearance.

This study shows targeted dephosphorylation of phospho-Tau at the endogenous level promotes its association with microtubules.

This paper develops scalable human neuron models of Alzheimer's disease to reveal mechanisms linking Tau fibrillization to synaptic dysfunction and identifies therapeutic targets.

This study shows that Drosophila with APOE4 variants exhibit AD-like phenotypes under stress and metabolic challenges, supporting a multi-hit model of disease.

This study compares the effects of nSMase and SPT inhibitors on Alzheimer's-like pathology in mice, finding that nSMase inhibition reduces neuropathology while SPT inhibition worsens it.

This study shows that APOE 4/4 genotype leads to dysfunctional and inflammatory astrocytes with impaired maturation and altered glutamate/Aβ handling in hiPSC-derived cultures.

This study shows that C4 deficiency reduces amyloid plaques and neuroinflammation in a mouse AD model, suggesting C4's role in glial reactivity and pathology.

The paper characterizes the AppSAA knock-in mouse model, showing it recapitulates age-dependent Alzheimer's disease phenotypes and provides a tool for preclinical research.

This study identifies cyclic peptide ligands targeting CAPON, showing reduced neuronal toxicity and tau phosphorylation under Alzheimer's disease stress conditions.

The paper identifies individuals with extreme polygenic risk scores (PRS) for Alzheimer's disease (AD) and shows they have significantly elevated AD risk across multiple ancestries and APOE diplotypes.

This study investigates how DNAJB6b binds to Aβ42 fibrils and inhibits amyloid elongation, providing a quantitative mechanism for its role in suppressing amyloid formation.

This study shows that mTOR inhibition reduces cerebrovascular Aβ accumulation and improves cognitive function in a mouse model of Alzheimer's disease with cerebral amyloid angiopathy.

This study investigates how deamidation at Q15 or N27 in Aβ-42 affects its aggregation and microglial immune response, finding reduced inflammation and altered CD68 expression.

This study shows that fingolimod worsens T cell infiltration and tau pathology in a mouse model of tauopathy, despite reducing peripheral T cells.

This study shows ApoE4 impairs astrocyte lipid droplet formation by disrupting endolysosomal function and demonstrates that PCSK9 can restore lipid droplet formation by preventing ApoE4 internalization.

The paper evaluates a seven-protein plasma panel across brain proteomics cohorts to show its association with AD proteomic changes.

This study investigates how the pentapeptide SKGQA cleaves multiple sites on amyloid-beta by using hydrophobic anchoring and stochastic catalytic targeting.

This study identifies a consistent proteomic signature of APOE ε4 across plasma and CSF, revealing cell-type-specific molecular effects in brain tissues associated with Alzheimer's disease risk.

This study shows that modulating neuronal cell cycle re-entry at a later age prevents Alzheimer's disease-related pathologies and highlights its relevance to late-onset AD.

This study identifies small-molecule inhibitors of the tau-LRP1 interaction using biochemical assays and high-throughput screening, showing reduced tau uptake in cellular assays.

This study determines the structure of the DC11 antibody and maps its epitope on truncated tau proteins using crystallography and computational methods.

This study shows melanin suppresses Aβ42 aggregation and toxicity in vitro and in a cell model, suggesting potential therapeutic applications for Alzheimer's disease.

This study shows that tau isoform balance regulates axon initial segment maturation, excitability, and transport, linking cytoskeletal organization to neuronal function.

This study shows that pathogenic tau in the locus coeruleus causes hyperactivity and neuropsychiatric symptoms similar to early Alzheimer's disease in mice.