Alzheimer's disease research and treatments

The paper identifies miR-7a-Klf4 as a regulator of neuroinflammation and ferroptosis in Alzheimer's disease and shows its therapeutic potential.

This study shows that amyloid pathology reduces neuronal dynamic range and impairs spatial coding in an Alzheimer's mouse model.

This study shows that increasing SORLA levels in aged tauopathy mice reduces multiple pathological effects, including tau phosphorylation, inflammation, and synaptic dysfunction.

The paper identifies transcriptional changes in interneurons across Alzheimer's disease stages in mice, revealing disease progression markers and potential therapeutic targets.

This study performs a sex-stratified transcriptomic meta-analysis of Alzheimer's disease to identify sex-specific and sex-dependent gene expression differences and potential drug targets.

This study identifies CK2 as a regulator of tauopathy by modulating tau phosphorylation, neuroinflammation, and synaptic dysfunction in mice.

This study shows that clearing tau proteins in C. elegans reverses neuronal dysfunction in both young and aged worms, suggesting potential for AD therapies targeting soluble tau.

This paper designs an orally bioavailable small molecule that targets RNA to reduce 4R tau protein abundance and alleviate disease phenotypes in a mouse model.

This study shows that FGFR1 agonists like FGF1 and FGL improve cognitive function and reduce pathology in an Alzheimer's disease mouse model.

This study shows that PSEN1 mutations disrupt regulated intramembrane proteolysis in astrocytes, leading to enhanced inflammatory responses and contributing to familial Alzheimer's disease progression.

This study shows that pathological tau spreads from the olfactory epithelium to brain regions in AD models and suggests targeting the olfactory epithelium to slow tauopathy progression.

This study uses scRNA-seq and network analysis to identify cell-type-specific transcriptional changes in Alzheimer's disease, revealing dysregulation in neurons and key roles of vascular cells.

The paper identifies distinct protein interactors of Tau-seed in AD across species and brain regions, highlighting functional differences in Tau propagation.

This study identifies APOE4-dependent metabolic changes in brain cells, showing increased glycolysis and mitochondrial dysfunction in neurons and astrocytes.

This study shows that overexpressing APPL1 in neurons causes AD-like endosomal and synaptic dysfunction, cholinergic neurodegeneration, and memory deficits in mice.

This study identifies the Aβ-HMGB1 complex as a pathogenic factor in advanced Alzheimer's disease, showing it causes neuronal damage and that targeting HMGB1 improves symptoms in mouse models.

This study shows that reactive astrocytes in Alzheimer's disease use glutamine metabolism to worsen amyloid pathology, and blocking this process reduces amyloid burden in mice.

This study shows HSV-1 infection induces Aβ clustering and neurodegeneration pathways in iPSC-derived neurons, supporting the pathogen infection hypothesis for Alzheimer's disease.

The paper identifies differences in post-translational modifications of amyloid-β isoforms between vascular deposits and parenchymal plaques in Alzheimer's disease.

The paper uses genetic perturbation and machine learning to analyze the energetics of amyloid beta nucleation, revealing its genetic architecture and transition state structure.

This study uses molecular dynamics simulations to analyze how phosphorylations of tau-R2 affect its binding to tubulin and the stability of the tau-microtubule interface.

This study shows that reducing SIRT2 in microglia worsens cognitive decline and amyloid pathology in Alzheimer's disease models.

This study shows that Ydj1, a heat shock protein 40, prevents amyloid fibril formation by promoting heterotypic phase separation of tau through electrostatic and hydrophobic interactions.

This study shows that gut miRNA depletion in App-knock-in mice alters microbiome composition, reduces Aβ load, and induces anxiety, suggesting miRNA manipulation could influence AD pathogenesis.

The paper identifies early transcriptional changes in neuronal subtypes in Alzheimer's disease using single-nucleus RNA data, revealing distinct programs linked to vulnerability and resilience.

This study examines PNOC and OPRL1 expression in Alzheimer's disease, finding sex differences and associations with psychiatric symptoms and circadian disruption.

The paper shows that high reelin expression in alECLII neurons promotes A{beta}42 accumulation, leading to early neuronal demise in Alzheimer's disease.

The paper develops STARFISH to visualize endogenous Tau translation and degradation in neurons, revealing spatial regulation and neuroproteasome-mediated degradation of Tau in dendrites.