Alzheimer's disease research and treatments

This study shows that NMNAT2 loss disrupts APP processing in neurons by causing redox failure and proteostasis disruption, with SARM1 playing a key role in this process.

This study uses patient-derived tau aggregates to induce disease-specific tauopathy features in human cells, revealing distinct pathological responses across tau strains.

The paper shows the exocyst regulates APP trafficking and amyloid-beta generation in neurons, with insulin signaling shifting exocyst activity away from APP to GLUT4.

This study identifies RSK1 as a central mediator of Tau phosphorylation in response to HIV and cocaine exposure, revealing a GSK3β-independent mechanism.

This study shows that human KL haplotypes FC and VS cause widespread transcriptomic changes in mouse brains at 12 months old, affecting mitochondrial, ribosomal, and synaptic functions, and linking them to Alzheimer's Disease pathogenesis.

The paper reconstructs the Alzheimer's disease neurodegenerative cascade in human L2/3 excitatory neurons using single-nucleus RNA sequencing data from multiple datasets.

This study identifies RUNX1 and YY1 as master transcription factors modulating neuronal fate and energy metabolism in Alzheimer's disease using patient-derived induced neurons and post-mortem brain data.

This paper describes the discovery and validation of C273, a mitochondrial complex I modulator that reduces Alzheimer's disease pathology by enhancing cellular resilience through AMPK-mediated pathways.

This study introduces FD-MD simulations to show that condensate interfaces enhance amyloid nucleation through β-motifs and molecular flux, leading to different growth morphologies and aging trajectories.

This study compares the effects of PSEN1 and PSEN2 knockout in iPSC-derived brain cells, finding distinct impacts on endo-lysosomal systems and APP cleavage.

The paper examines APOE ε4 allele frequencies across 9,524 individuals from 83 Indian populations, revealing significant variation and associations with lipid phenotypes.

This study maps stage-dependent tau post-translational modifications across Alzheimer's disease progression, revealing early phosphorylation and later ubiquitination events associated with tau aggregation.

The paper shows that inducing a hibernation-like brain state in AD mice slows amyloid plaque accumulation and reduces neuroinflammation without targeting specific pathways.

The paper investigates the effects of tau oligomers on sharp-wave ripples in mouse and human hippocampal slices, finding reversible impairments in SWR parameters depending on species and tau preparation.

This study identifies terazosin as a drug that reverses AD-related molecular signatures and preserves noradrenergic circuits in a sex-dependent manner in a rat model of Alzheimer's disease.

This study examines how alpha-synuclein affects amyloid-tau and tau-cognition relationships in Alzheimer's disease, finding modest cross-sectional associations but no significant longitudinal effects.

The paper designs AI-guided nanobodies targeting the VQIVYK motif of tau, showing strong binding to synthetic tau and Alzheimer's brain tissue.

Deleting TNFR1 in astrocytes improves memory in aged Alzheimer's mice by rebalancing hippocampal circuitry excitability through synaptic pathway changes.

This study characterizes cell-type-specific transcriptomes across APOE genotypes in Alzheimer's disease using single-nuclei RNA sequencing, revealing APOE4-associated changes in excitatory neurons and microglia.

The paper identifies the phosphoS655 APP interactome in neuronal differentiation, showing it contributes to neuritogenesis through specific protein interactions.

The paper identifies TMEM106B fibril accumulation as a shared mechanism in neurodegeneration linked to genetic variants in TMEM106B and GRN.

This study shows that iron toxicity enhances cell-type specific amyloid beta proteotoxicity in C. elegans at low temperatures by disrupting energy homeostasis and mitochondrial function.

The paper investigates the role of LACTB in Alzheimer's disease risk through Mendelian Randomization and experimental models, finding reduced LACTB expression lowers AD risk and increases succinylcarnitine levels.

This study shows that overexpressing BiP in the hippocampus of 3xTg AD mice improves cognitive performance and reduces Aβ and Tau pathology.

The paper identifies cis-regulatory elements and genetic variation effects in the MAPT locus using MPRA and CRISPRi in neuronal and HEK293FT cells.

This study shows that deleting GFAP and Vimentin in astrocytes reduces early synaptic and cognitive dysfunction in Alzheimer's mice by improving protein synthesis and astrocyte function.

The paper develops a cross-species translation framework to identify therapeutic targets for late-onset Alzheimer's disease using mouse models and human data.