Alzheimer's disease research and treatments

The paper describes a method to microdissect and culture adult entorhinal layer II neurons from AD model mice, showing they remain viable and functionally active for over two months.

This study examines APOE Christchurch carriers in UK Biobank to assess their risk of Alzheimer's disease, cardiovascular disease, and dyslipidemia, finding lower apoB levels and reduced AD risk.

This study identifies truncated Aβ fragments that form SDS-stable, low molecular weight oligomers impairing synaptic plasticity and evading conventional antibodies.

This study uses single-nucleus RNA-sequencing to analyze astrocyte transcriptomic changes across the spatiotemporal progression of Alzheimer's disease, revealing gene expression trajectories and heterogeneity.

This study shows ApoE isoforms modulate neuroproteasome function, affecting Tau aggregation thresholds and contributing to Alzheimer's disease pathology.

This study identifies JUN upregulation as a driver of transposable element mobilization, innate immune activation, and impaired neurogenesis in Alzheimer's disease.

The paper reports the atomic structure of glucagon amyloid fibrils using cryo-EM, revealing a dimeric architecture and distinct from previous models.

This paper describes the generation of a hybrid Alzheimer disease mouse model and shows it reduces cognitive and neuronal deficits compared to APP knock-in mice.

This study shows that the Swedish FAD mutation disrupts axonal transport by increasing dynactin recruitment to APP motor assemblies, leading to retrograde movement and accumulation of APP in the soma.

The paper investigates circuit-specific vulnerability in the default mode network (DMN) in Alzheimer's disease, finding that dysfunction is restricted to in-DMN projecting circuits despite widespread amyloid burden.

This study investigates the role of SUMO2/3 modification in mitigating Tau-induced synaptic and cognitive dysfunction in disease models.

This study reveals the in-tissue molecular architecture of β-amyloid fibrils in a mouse model of Alzheimer's disease, showing their arrangement in lattices and their structural differences due to the Arctic mutation.

The paper identifies small molecule inducers of miR-132 in human iPSC-derived neurons using HTS-HTS, showing neuroprotective effects against neurodegenerative phenotypes.

This study introduces S-BEAM, a semi-supervised ensemble method to prioritize non-coding variants and their target genes in microglia for Alzheimer's disease, identifying 11 risk variants and proposing 37 for further study.

The paper uses scRNA-seq to analyze peripheral blood mononuclear cells from MAPT carriers and controls, finding reduced CX3CR1 and nonclassical monocytes associated with tau pathology.

The paper shows that ELA-associated increased chromatin accessibility and expression of APOE4 in astrocytes contribute to higher AD risk in APOE4/4 carriers.

This paper develops a non-human primate model of Alzheimer's disease by overexpressing human tau in the hippocampus, showing AD-like pathological features.

This study shows that localized APP pathology in hippocampal CA3 cells leads to altered neuronal firing patterns in connected regions, suggesting disease progression can occur through physiological dysfunction rather than just spreading pathology.

This study shows that SPPL2b affects APP cleavage and has biphasic Aβ-mediated expression in Alzheimer's disease, suggesting it as a potential drug target.

This paper develops a hierarchical Bayesian model to predict amyloid-beta accumulation from biomarker candidates using mouse behavioral data, showing improved prediction when multiple features are used.

This study identifies naturally occurring Alzheimer's disease in aged rhesus monkeys, showing cognitive impairments and AD pathological hallmarks.

The paper identifies JMJD6 and other key drivers of Alzheimer's disease using predictive network analysis and validates their effects on amyloid-beta and tau pathology in human neurons.

The paper identifies proteomic features of resilience to Alzheimer's disease, finding lower soluble Aβ levels and specific protein interactions in brain regions associated with resistance to dementia.

The paper investigates how the C112R mutation in ApoE4 causes aggregation and shows that tramiprosate reduces this aggregation.

This paper predicts Amyloid-β concentrations in Alzheimer's disease using a machine learning autoregressive model constrained by structural connectivity, achieving lower prediction error than existing methods.

This study shows fasudil reverses gene expression patterns associated with neurodegenerative disease in Alzheimer's model mice.

This study shows that APOE4 astrocytes increase neuronal metabolic stress in the presence of amyloid-β compared to APOE3 astrocytes.

This study shows that somatostatin reduces Aβ plaque formation in aged mice by inhibiting Aβ aggregation, independent of neprilysin.

This study investigates the impact of cellular prion protein expression on disease progression in two Alzheimer's disease mouse models, finding contradictory results that may be explained by differences in Aβ oligomer conformation.