Alzheimer's disease research and treatments

A single injection of anti-PD-L1 blocking antibody induces a transient reduction in tau pathology in P301S (PS19) mouse model of tauopathy

A single anti-PD-L1 injection reduces tau pathology and cognitive deficits in P301S mice but the effect is transient.

Harnessing cGAS-STING signaling to counteract the genotoxic-immune nexus in tauopathy

This study identifies a cGAS-STING signaling loop driving neuroinflammation and tau pathology in tauopathies, showing its disruption can alleviate disease symptoms.

Metabolic Trans-Omic Analysis Reveals Key Regulatory Disruption of Energy Metabolism in Alzheimer's Disease

The paper integrates multi-omic data from Alzheimer's disease patients to reveal coordinated downregulation of energy-producing metabolic pathways.

Early Aβ-induced changes in the enteric nervous system and gut: structure, function, and motility

This study examines the acute and prolonged effects of Aβ on enteric neurons and intestinal motility, finding increased excitability and contractility initially, followed by structural and synaptic changes after 72 hours.

Resveratrol enhances associative learning and memory function in C. elegans Models of Alzheimer's Disease: A chemotaxis-based behavioral analysis

This study shows resveratrol improves chemotaxis in Alzheimer's model worms, suggesting potential therapeutic benefits for neurodegenerative diseases.

A multi-ancestry polygenic risk score for Alzheimer disease is associated with cognitive decline, hippocampal atrophy and neuropathological hallmarks in diverse populations

This paper develops an APOE-independent polygenic risk score for Alzheimer's disease that shows associations with cognitive decline and neuropathological markers across diverse populations.

Rare bioactive tau oligomers from Alzheimer brain support both templated misfolding and fibril formation

The paper identifies rare bioactive tau oligomers in Alzheimer's brain that can induce templated misfolding and fibril formation, distinguishing them from non-bioactive oligomers.

Electric Field-Induced Destabilization and Surface Modulation of Aβ42 Fibrils in Molecular Simulations: Theoretical Implications for DC Stimulation in Alzheimer's Disease

This paper uses molecular dynamics simulations to study how static electric fields affect Aβ42 fibrils, showing they destabilize fibrils by altering surface properties and reducing secondary nucleation.

Beyond Alzheimer's story: how an engineered molecule gained an endogenous essence

The paper identifies HAEE as an endogenous blood plasma component reduced in Alzheimer's patients, suggesting it as a biomarker and potential therapeutic agent.

The protective PLCG2 variants delay Alzheimer's disease onset age in APOE ϵ4 carriers

The paper examines how protective PLCG2 variants delay Alzheimer's onset in APOE ε4 carriers and identifies associated plasma biomarkers.

Monomer binding modes of small molecules that modulate the kinetics of hIAPP amyloid formation

This study uses molecular dynamics simulations to investigate how small molecules bind to hIAPP monomers and affect amyloid formation kinetics.

BAG3 coordinates astrocytic proteostasis of Alzheimer's disease-linked proteins via proteasome, autophagy, and retromer complex interactions

This study identifies BAG3's role in astrocytic proteostasis in Alzheimer's disease by showing its interactions with autophagy, proteasome, and retromer components, and its impact on Aβ clearance.

The effect of quercetin on the fluorescent intensity of neurofibrillary tangles that correspond to Alzheimers disease within Drosophila melanogaster

This study investigates quercetin's effect on neurofibrillary tangle intensity in Drosophila melanogaster with Alzheimer's disease and finds no significant effect.

Insights into structures of peptide aggregation nuclei from concentration dependence of lag time

The paper analyzes peptide aggregation lag time as a function of concentration to determine critical nucleus size and improve models of amyloid formation.

Design of Tau Aggregation Inhibitors Using Iterative Machine Learning and a Polymorph-Specific Brain-Seeded Fibril Amplification Assay

The paper develops an in vitro tau aggregation assay combined with machine learning to identify polymorph-specific tau inhibitors, validated in a Drosophila model.

Generation of a recombinant GST-Tau antigen for indirect ELISA in evaluating Alzheimer`s disease vaccines

The paper develops a method to produce a recombinant GST-Tau antigen for use in indirect ELISA to detect anti-Tau antibodies in Alzheimer's disease vaccine research.

Sex dependent effect of amyloidosis on functional network hub topology is associated with downregulated neuronal gene signatures in the APPswe/PSEN1dE9 double transgenic mouse

The paper examines how amyloidosis affects functional network hub topology and gene expression in male and female APP-PS1 mice, finding sex-dependent changes in connectivity and gene signatures.

Clearing truncated tau protein restores neuronal function and prevents microglia activation in tauopathy mice

This study shows that targeting truncated tau protein with a monoclonal antibody reduces tau levels, improves neuronal function, and decreases microglia activation in tauopathy mouse models.

Therapeutic assessment of a novel mitochondrial complex I inhibitor in in vitro and in vivo models of Alzheimer's disease

The paper assesses a novel mitochondrial complex I inhibitor, C458, in vitro and in vivo, showing it protects against Aβ toxicity, improves brain energetics, and reduces inflammation in Alzheimer's disease models.

ACE1 Does Not Influence Cerebral Aβ Degradation or Amyloid Plaque Accumulation in 5XFAD Mice

This study investigates whether ACE1 influences Aβ degradation or amyloid plaque accumulation in 5XFAD mice, finding no effect on amyloid burden or neuroinflammation.

Molecular Polymorphism of tau aggregates in Pick's disease

This paper uses micro-XRD and XRF to analyze tau aggregates in Pick's disease, finding distinct elemental compositions and fibril structures in different lesion types.

CNS-Tau Specific Antibodies Illuminate Disease Signatures Across Tauopathies

The paper develops and validates CNS-tau-specific monoclonal antibodies for use in neuropathology and plasma biomarker assays across Alzheimer's disease and primary tauopathies.

Kat5 cKO Biological Domain Signatures Align with Human Alzheimer Disease

The paper compares the transcriptome of Kat5 knockout mice to AD datasets, finding similar gene expression patterns and showing KAT5 localization in AD neurons.

Pathogenic tau inhibits synaptic plasticity by blocking eIF4B-mediated local protein synthesis

Sex-specific effects of fecal microbiota transplantation on TBI-exacerbated Alzheimer's pathology in mice

This study investigates how fecal microbiota transplantation (FMT) affects Alzheimer's pathology and neuroinflammation in male and female mice with traumatic brain injury, finding sex-specific outcomes.

Kinetic Model With Feedback Cycle for Age-Dependent Beta Amyloid Accumulation in Mice

The paper develops a kinetic model of A{beta} accumulation in Tg2576 mice to evaluate therapeutic interventions and highlights the role of feedback cycles in disease progression.

Targeted degradation of pathologic tau aggregates via AUTOTAC ameliorates tauopathy

This paper demonstrates that AUTOTAC, a targeted degradation approach, reduces tau aggregates and improves symptoms in tauopathy models and companion dogs.

Disease-specific tau polymorphs define unique protein interaction networks across proteinopathies

The paper identifies disease-specific tau polymorphs and their unique protein interaction networks in Alzheimer's, PSP, and DLB, revealing distinct molecular signatures and therapeutic targets.

Fluphenazine, an antipsychotic compound, ameliorates Alzheimer's disease by clearing amyloid beta accumulation in C. elegans

This study screens FDA-approved compounds in yeast and C. elegans to identify potential Alzheimer's disease treatments, finding that fluphenazine reduces amyloid-beta accumulation.

Neurodegeneration emerges at a cellular tipping point between aggregate accumulation and removal.

The paper identifies a cellular tipping point between aggregate accumulation and removal as a universal feature of neurodegeneration, validated through live-cell assays and super-resolution imaging.