Alzheimer's disease research and treatments

This study models amyloid-β plaque growth, finding that plaque size increases proportionally to the cube root of time and is limited by monomer production/degradation rates.

The paper shows ApoE modifies Aβ oligomers to a more toxic form, detectable in live cells, and presents a potential assay for AD drug discovery.

This study reports the atomic structures of phospho-mimetic tau fibrils, showing how specific phosphorylations lead to distinct aggregate formations.

The paper uses live-cell imaging to identify a drug candidate that restores microtubule regulation by targeting tau aggregation and phosphorylation in a tauopathy model.

The paper introduces Path2MR, a pipeline for 3D histology reconstruction without MRI, revealing distinct tau and amyloid-beta pathology gradients along the hippocampal axis in Alzheimer's Disease.

This study shows that reducing tau in human neurons decreases A beta toxicity, supporting the role of tau in Alzheimer's disease mechanisms.

The paper identifies two covalent inhibitors that disrupt the interaction between SYK's tandem SH2 domains and FCER1G phospho-ITAM, potentially beneficial for Alzheimer's disease therapy.

The paper determines the structure of amyloid-β (Aβ40) fibrils bound to lipids using cryo-EM, showing lipid binding and potential relevance to Alzheimer's disease pathogenesis.

The paper investigates CHRNA5's role in amyloid pathology in aging and Alzheimer's by analyzing genetic variants and cell-type expression in human brain tissue.

This study identifies Lag3 as a neuronal receptor for Tau preformed fibrils, essential for their uptake, propagation, and transmission in Tauopathies.

The paper identifies transmembrane protein 97 as a synaptic receptor for amyloid beta in human Alzheimer's disease using advanced microscopy and drug intervention studies.

This study shows that CT-KIBRA repairs synaptic plasticity and memory in tauopathy models by stabilizing PKMζ, without altering tau levels or preventing synapse loss.

This study systematically reviews and meta-analyzes tau phosphorylation levels in mouse models of familial Alzheimer's disease, finding age-dependent variations in hyperphosphorylation across different models.

The paper investigates DNA breaks in Alzheimer's disease brains, finding a loss of adaptive DNA breaks at nervous system genes despite an overall increase in DNA breaks.

This study shows that inhibiting C5aR1 reduces excessive synaptic pruning and synaptic loss in AD mouse models, improving LTP in an age and region-dependent manner.

This study examines how levetiracetam affects brain metabolic networks and transcriptomic signatures in 5XFAD mice, showing dose- and sex-dependent changes in gene expression and cerebral metabolism.

The paper identifies a pathogenic SORL1 variant, p.R953C, associated with Alzheimer's Disease and shows it impairs protein maturation and endosomal sorting.

This paper extends a deterministic Alzheimer's disease model by incorporating stochastic Markov processes, showing increased neuron death and decreased Tau and Amyloid beta production rates.

This study shows that glucocorticoids promote vesicle-free Tau secretion and trans-neuronal Tau spreading in the brain, contributing to Alzheimer's disease progression.

This study identifies a metabolic block in the TCA cycle in Alzheimer's disease neurons and shows that dimethyl succinate treatment rescues mitochondrial function and synapse loss.

This study shows ATP prevents protein aggregation and dissolves pre-formed aggregates, suggesting it could be a therapeutic agent for protein-aggregation diseases.

This paper develops a numerical model to simulate senile plaque development under limited amyloid-β monomer diffusivity, showing how plaque radius and aggregate concentrations depend on key dimensionless parameters.

This study shows that Aβ accumulation in a mouse AD model reduces nuclear pore complex function, leading to impaired nucleocytoplasmic transport and increased vulnerability to necroptosis.

This study investigates the proteomic and phosphoproteomic effects of DUSP4 overexpression in 5xFAD mice, revealing sex-specific molecular mechanisms and validating findings in human AD cohorts.

The paper shows Drosophila melanogaster resist trans-synaptic spread of human tau, suggesting they are not suitable for screening tau propagation modifiers.

This paper introduces OptoTau, an optogenetic tool that induces different tau aggregation forms in Neuro2a cells based on blue light exposure patterns.

The paper identifies gene co-expression modules driving pathway dysregulation in Alzheimer's disease using single-nucleus RNA-seq data from brain regions.

The paper investigates synaptic and dendritic changes in a mouse model of tauopathy, finding altered synaptic integration and dendritic restructuring associated with early-stage tau pathology.

This study shows that targeted brain-specific tauopathy in mice leads to skeletal muscle weakness and altered gene expression.