Alzheimer's disease research and treatments

This study identifies RHBDL4 as an enzyme that processes APP similarly to {eta}-secretase, generating A{eta}-like fragments in the ER without requiring other proteases.

The paper identifies genetic subtypes of Alzheimer's disease using PCA and biclustering, finding two disease-specific genetic signatures associated with cognitive decline and pathological markers.

The paper investigates early synaptic dysfunction and emotional behavior in AppNL-F mice, finding reactive astrocytes contribute to synaptic mistuning before Aβ plaques and are linked to depressive-like behavior.

The paper investigates how heparan sulfate-modified proteoglycans influence AD-related pathways by modulating presenilin function in human cells, mouse astrocytes, and Drosophila.

This study shows that DUSP6 overexpression in the dorsal hippocampus of male 5xFAD mice reduces amyloid load and improves memory, while also reducing neuroinflammation in both sexes.

The paper identifies PTPRS as a neuroprotective marker in Alzheimer's disease, showing associations with reduced tau pathology and synaptic degeneration, particularly in males.

This study shows that pathogenic tau increases mRNA translation rate early in disease by altering NMD and promoting translation of neurodegeneration-linked mRNAs.

This paper reports exploratory CSF proteomics data from a Phase 2 trial of CT1812 in Alzheimer's disease, identifying pharmacodynamic biomarkers and mechanistic insights.

This study shows that male and female 3xTg-AD mice have different disease trajectories, with males showing more inflammation and females more neuropathology, mirrored in human Alzheimer's patients.

This study shows that Aβ can form mixed polymorphs with different seeds, deviating from its typical parallel β structure, and highlights the complexity of Aβ aggregation in Alzheimer's disease.

The paper uses cryo-EM to show that tau filaments in Down syndrome share the same structure as those in Alzheimer's disease.

This study uses QSLIP to map amyloid-beta oligomer membrane insertion, finding toxicity correlates with amino-terminal penetration depth.

The paper examines mitochondrial alterations in fibroblasts from Alzheimer's disease patients and links them to clinical hallmarks and cognitive decline.

The paper identifies altered glia-neuron communication in Alzheimer's disease using snRNA-seq, revealing dysregulation of WNT, p53, and NFkB signaling in inhibitory neurons.

This study reconstitutes and characterizes the C99 domain of APP in nanodiscs using multiple biophysical methods.

This study shows APOE4 increases mitochondrial ATP production in neurons compared to other APOE isoforms, suggesting a gain-of-function effect on neuronal energy metabolism.

This study uses SMOLM to analyze A{beta}42 fibril architecture and dynamics, finding that order and heterogeneity correlate with growth and decay.

The paper shows that apoE isoforms modulate Aβ aggregation, clearance, and toxicity in Alzheimer's disease, with implications for therapeutic strategies.

This study shows that sleep disruption accelerates cognitive decline in male P301S Tau mice but not females, without directly causing synaptic Tau pathology.

The paper shows tau accumulates around blood vessels in Alzheimer's disease brains and is linked to tau tangle pathology.

The paper reports cryo-EM structures of γ-secretase complexes with and without Aβ46, revealing structural insights into Aβ processing and APH-1B's role.

This study shows tau fibrils enter cells via endocytosis, accumulate in lysosomes, cause membrane damage, and nucleate cytosolic tau at lysosomes.

BD10-2, a TrkB/C partial agonist, improves memory and LTP deficits in Alzheimer's mice by modulating synaptic signaling and microglial transcriptomic changes.

The paper analyzes genetic diversity's effect on brain composition in an Alzheimer's disease mouse model using an enhanced QUINT workflow.

The paper investigates the properties and expression patterns of Big tau in the visual system, revealing its unique isoform structure and developmental expression switch.

This study shows that particulate matter exposure in vitro causes amyloid beta plaques and neurite shortening in neuron-like cells, resembling Alzheimer's disease features.

This study shows that Urolithin A improves cognitive function and restores mitophagy and lysosomal functions in Alzheimer's disease mouse models.

This study shows that amyloid β accelerates age-related protein insolubility in C. elegans and links this process to neurodegenerative and age-related diseases through proteomics and GWAS.

This study characterizes molecular and synaptic changes in a mouse model of late-onset Alzheimer's disease under different dietary conditions, showing age-related brain volume loss and cognitive deficits.