Alzheimer's disease research and treatments

The paper investigates how phosphorylation near the pT181 epitope affects the affinity of pT181-tau antibodies, finding that phosphorylation at S184 or S185 can completely eliminate antibody binding.

The paper models apoE interactions with Alzheimer's amyloid-beta fibrils, showing conformational changes enable binding and suggesting a mechanism for apolipoprotein-amyloid co-deposition.

This study shows ZCCHC17 regulates RNA splicing in neurons and its dysfunction contributes to splicing abnormalities in Alzheimer's disease, with potential therapeutic implications.

This study identifies a common oligomerization pathway for Aβ42 stabilized by SDS and DPC micelles, revealing structural and stabilizing mechanisms.

This study shows that TFEB-v-ATPase signaling regulates lysosomal function and microglial activation in tauopathy by impairing lysosomal acidification and altering microglia responses.

The paper presents cryo-EM structures of Aβ fibrils from Alzheimer's disease mouse models and compares them to human fibrils.

This study uses molecular dynamics simulations and mass spectrometry to model how γ-secretase cleaves Notch1, revealing structural dynamics and substrate interactions.

This study examines gastrointestinal redox biomarkers in Tg2576 mice, finding differences between presymptomatic and symptomatic stages and effects of D-galactose treatment on redox homeostasis and behavior.

This study shows hyperphosphorylated tau causes ER stress and inflammation, which are reduced by apomorphine and HO-1 overexpression.

The paper identifies a conserved role for APP in proteostasis during aging through genetic and multi-omics analyses in Drosophila and human models.

This study identifies key copy number variations and genes associated with longevity in late-onset Alzheimer's disease patients using causality network analysis of multi-omics data.

This study shows that chronic XBD173 treatment improves cognitive deficits and reduces AD pathology in mice via TSPO, with TSPO being necessary for its procognitive effects.

The paper introduces GenomicsDB, a public knowledgebase for Alzheimer's disease genetic datasets and annotations, enabling data sharing and discovery through harmonized GWAS summary statistics and functional annotations.

This study uses progerin to accelerate AD phenotypes in neural progenitor cells with FAD mutations, showing increased tau phosphorylation, amyloid plaques, and cell death within weeks.

This study shows that human Aβ42 inhibits γ-secretase, leading to substrate accumulation and neuronal dysfunction, suggesting a feedback mechanism in Alzheimer's disease.

This study identifies MSN and CD44 as potential therapeutic targets for Alzheimer's disease by developing inhibitors of their interaction through structural and chemical screening.

The paper investigates how the APP ectodomain regulates gamma-secretase processivity and A beta peptide length, identifying it as a target for Alzheimer's disease therapies.

This study identifies novel Alzheimer's disease genes and epistasis using machine learning GWAS tools, capturing more phenotypic variance and discovering new loci with epistatic interactions.

This study shows genetic background affects the proteome in 5XFAD AD mouse models, with some disease-related modules influenced by genetic background while others are not.

This paper proposes an AD risk gene prediction framework using spatial and temporal gene expression data with SVM, identifying 15 high-probability risk genes.

The paper uses infrared spectroscopic imaging to show that amyloid plaques in Alzheimer's disease contain antiparallel beta-sheet structures, linking in vitro findings to in vivo pathology.

The paper investigates the origins of astrocytic tau aggregates in tauopathies and finds that astrocytes preferentially uptake neuronal 4R tau, which is impaired by inflammation and nutritional stress.

The paper determines cryo-EM structures of Tau filaments from transgenic mice models and identifies differences compared to human Tau filaments.

The paper investigates how Tau protein affects epigenetic regulation of cellular senescence by analyzing transcriptome data from Tau-depleted cells.

This study shows that DKK3, a Wnt antagonist elevated in Alzheimer's disease, causes synaptic loss and memory impairment, but its knockdown restores synapse integrity and memory in a mouse model.

This study shows that retaining proteins in the ER can rescue Aβ toxicity in Drosophila and mouse models, suggesting a potential therapeutic strategy for Alzheimer's disease.

This study shows that increasing pyruvate import in neurons rescues dementia-like phenotypes in fly models by clearing toxic protein deposits.

This study shows that TMEM184B loss in mice affects synaptic gene expression and anxiety-related behavior, suggesting a link to neurodevelopmental disorders rather than dementia.

The paper uses proteomic analysis of patient iPSC-derived brain cells and post-mortem hippocampal tissue to study early AD pathogenesis and prion-like spread.

The paper examines excitability changes in the medial entorhinal cortex of 3xTg mice at early and late stages of Alzheimer's disease pathology, finding hyperexcitability in specific cell types and altered synaptic ratios.