Alzheimer's disease research and treatments

The Drosophila wing is a high-throughput and versatile screening tool for Tau-mediated disease mechanisms and drug discovery.

This paper describes using Drosophila wing discs to study Tau-mediated disease mechanisms and screen for neuroprotective drugs, showing that human Tau causes cell death and that NAP reduces toxicity.

From Correlation to Causation: Cell-Type-Specific Gene Regulatory Networks in Alzheimer's Disease

This study constructs cell-type-specific gene regulatory networks in Alzheimer's disease using single-nucleus transcriptomics and genotype data, identifying both established and novel regulatory elements.

Soluble SORL1 in cerebrospinal fluid as a marker for functional impact of rare SORL1 variants.

The paper measures soluble SORL1 (sSORL1) in CSF to assess functional impact of rare SORL1 variants, finding lower sSORL1 in carriers of pathogenic variants.

The Highly Selective 5-HT2B Receptor Antagonist MW073 Mitigates Aggressive Behavior in an Alzheimer Disease Mouse Model.

This study shows that the 5-HT2B receptor antagonist MW073 reduces aggressive behavior in an Alzheimer's disease mouse model.

Small tau aggregates exhibit disease-specific molecular profiles across tauopathies

The paper identifies disease-specific molecular profiles of small tau aggregates across different tauopathies using single-molecule assays.

Matching Heterogeneous Cohorts by Projected Principal Components Reveals Two Novel Alzheimer's Disease-Associated Genes in the Hispanic Population

Molecular Signatures of Resilience to Alzheimer's Disease in Neocortical Layer 4 Neurons

The paper identifies molecular signatures of resilience in neocortical layer 4 neurons in Alzheimer's disease using single-cell and spatial transcriptomics.

Cytomegalovirus-induced T cell responses accelerate Alzheimer's disease progression in mice

This study shows that MCMV infection accelerates AD-like features in mice, with T cell responses playing a key role in disease progression.

APPNL-F knock-in Alzheimer's Disease model mice reveal etiological convergence of aging and amyloidosis

This study characterizes the early stages of amyloidosis and neuroinflammation in APPNL-F AD model mice, revealing a link between microglial senescence and disease progression.

Riluzole shifts glial responses to protect synapses and memory in Aβ oligomer-treated rats

This study shows riluzole improves memory and synaptic function in Aβ oligomer-treated rats by promoting glial remodeling and reducing neuronal Aβ burden.

Assessing the repurposing potential of disease-modifying antirheumatic drug targets to reduce Alzheimer's disease risk: a pQTL-based Mendelian randomization and colocalization analysis

This study uses pQTL-based Mendelian randomization and colocalization to assess if DMARD targets reduce Alzheimer's disease risk, finding only FCGR3B shows increased risk with higher plasma levels.

Dynamical Aβ-Tau-Neurodegeneration Model Predicts Alzheimer's Disease Mechanisms and Biomarker Progression

The paper introduces a dynamical ATN model to simulate and predict the spatiotemporal progression of Aβ, tau, and neurodegeneration in Alzheimer's disease using multimodal imaging data.

A HaloTag-4R-Tau Pulse-Chase Sensor Reveals Neddylation Inhibition Promotes Degradation of Tau in iNeurons

The paper develops a HaloTag-4R-Tau sensor to study tau clearance in iNeurons and identifies Neddylation inhibition as a method to promote tau degradation.

Autophagy activators normalize aberrant Tau proteostasis and rescue synapses in human familial Alzheimer's disease iPSC-derived cortical organoids

This study uses human iPSC-derived cortical organoids to model familial Alzheimer's disease and shows that autophagy activators reduce pathological Tau and Aβ accumulation and rescue synaptic loss.

Elevated Na+/K+ Ratio in Alzheimers Disease: A Potential Biomarker for Braak Stage

This study investigates the Na+/K+ ratio in Alzheimer's disease and finds it is elevated in thalamus and CSF, correlating with Braak tangle stage.

Dynamic conformational ensembles of soluble Tau encode neuronal toxicity prior to aggregation

This study identifies dynamic conformational states of soluble Tau that precede aggregation and correlate with neuronal toxicity in Alzheimer's disease and related tauopathies.

Electro-Calcium uncoupling precedes neurodegeneration in Alzheimers disease

This study shows that electro-calcium uncoupling in endothelial cells precedes neurodegeneration and cognitive decline in 5xFAD mice.

Non-viral vasculogenic reprogramming restores cognition and mitigates pathology in Alzheimer's disease

This study shows that non-viral reprogramming of fibroblasts to vasculogenic cells improves cognition and reduces pathology in Alzheimer's disease mouse models.

The loss of Tau in the adult brain triggers neuroplastic, epigenetic and behavioral deficits

This study shows that loss of normal Tau function in the adult brain causes neuronal atrophy, epigenetic changes, and cognitive/mood deficits, which can be reversed by Tau re-expression or epigenetic correction.

Early synaptic pathology is associated with small tau aggregates in Alzheimer's disease

The paper examines tau aggregates in Alzheimer's disease synaptosomes, finding that small tau aggregates are associated with early synaptic pathology.

Artificial microRNAs targeting Tau enable post-symptomatic functional recovery in aged tauopathy mice

This study shows that artificial microRNAs targeting Tau can improve cognitive and neuronal function in aged tauopathy mice after symptoms have developed.

Dysregulated RNA G-quadruplex binding proteins reveal shifted stress responses in Alzheimer's Disease

The paper identifies dysregulated RNA G-quadruplex binding proteins (RG4BPs) in Alzheimer's Disease, linking their altered expression to glial cell dysfunction and stress state shifts.

Dyrk1a inhibition with the Novel Compound DYR533: A Cross-Disease Therapeutic Strategy Targeting Amyloidosis, Tau Pathogenesis, and Neuroinflammation

This study shows that inhibiting Dyrk1a with the compound DYR533 reduces tau pathology, neuroinflammation, and amyloidosis in mouse models of neurodegenerative diseases.

Tau oligomers modulate synapse fate by eliciting progressive bipartite synapse dysregulation and synapse loss

This study shows that tau oligomers cause progressive synapse dysfunction by initially weakening both presynaptic and postsynaptic components, followed by synaptic loss.

Identification of Chlamydia pneumoniae and NLRP3 inflammasome activation in Alzheimer's disease retina

The paper identifies Chlamydia pneumoniae infection and NLRP3 inflammasome activation in Alzheimer's disease retinas, linking them to disease progression and cognitive impairment.

Agomelatine drives sex-specific neuroprotection and reduced pathology in rat and human Alzheimer's models

This paper identifies agomelatine as a disease-modifying candidate for Alzheimer's disease, showing sex-specific neuroprotection and reduced pathology in both rat and human models.

The core herpes simplex-1 fusion complex drives cell-to-cell spreading of pathological Tau

This study shows HSV-1 fusion proteins enable cell-to-cell spread of pathological Tau, suggesting latent HSV-1 infection may contribute to neurodegenerative disease progression.

Amelioration of symptomatic Alzheimer's Disease after selective impairment of p75NTR function in adult forebrainexcitatory neurons

This study shows that impairing p75NTR function in adult forebrain excitatory neurons reduces AD pathology and cognitive deficits, even when applied during advanced disease stages.

m6A modification and prion-like domain proteins converge to dysregulate Neuronal RNA Granules in Alzheimer s disease

This study identifies dysregulation of m6A modification and prion-like domain proteins in Neuronal RNA Granules as potential contributors to Alzheimer's disease pathogenesis.

Motor deficits in the McGill-R-Thy1-APP transgenic rat model of Alzheimer's Disease

This study evaluates motor deficits in McGill-R-Thy1-APP rats, finding genotype and sex effects on motor behavior but not on spontaneous alternation.