Luc Buée

This study identifies AETA peptide as a novel contributor to synaptic dysfunction in Alzheimer's disease, particularly in females, through post-mortem analysis and a mouse model.

The paper uses single-domain antibodies to investigate how different tau domains influence RNA-induced tau liquid-liquid phase separation, identifying a proline-rich domain as critical for condensation.

This study identifies and characterizes a novel N-terminally acetylated Tau variant that accumulates in AD models and patients, exacerbates pathology, and is a potential therapeutic target.

This study shows that p97/VCP regulates APP metabolism by controlling its trafficking and autophagy-dependent degradation of APP-CTFs, linking it to Alzheimer's disease pathology.

This study shows that platelet concentrate-derived extracellular vesicles enhance adult hippocampal neurogenesis in both ex vivo and in vivo models.

This study shows that maternal high-fat diet during lactation accelerates tauopathy in THY-Tau22 mice, with sex-dependent effects where males are more affected earlier than females.

The paper screens patients with parkinsonism for RFC1 gene expansions and finds that Parkinson's disease and multiple system atrophy can be gateways to RFC1-related disorders.

The paper examines reduced SV2A levels in AD brain tissue and extracellular vesicles, linking them to amyloid-β, tau, and synaptic markers.

The paper identifies distinct proteomic signatures in brain-derived extracellular vesicles from 3R and 4R tauopathies, linking them to disease-specific cellular and molecular changes.

This study shows that impairing the AMPK-ULK1 cascade in Alzheimer's disease leads to mitochondrial dysfunction and AD-related changes, which are improved by metformin treatment.

The paper designs a 19-residue peptide that selectively induces aggregation of 4R tau over 3R tau, revealing structural and amino acid determinants of tauopathy propagation.

This study shows that tau-containing extracellular vesicles from neurons transfer tau to astrocytes, disrupting their mitochondrial function, with 3R tau being more damaging than 4R tau.

The paper identifies two novel LRRK2 variants associated with familial Parkinson's disease and shows they alter phosphorylation and kinase activity.

This study shows that injecting human Alzheimer's brain extracts into mice with amyloid-beta plaques induces tau pathology, memory deficits, and synaptic loss, with neuritic plaques linked to synaptic impairment.

This study shows that inhibiting ENT1 with J4 reduces Tau-mediated neurodegeneration in a mouse model by improving energy homeostasis and mitigating immune responses.

The paper identifies AD risk genes that influence microglia response to amyloid-β but not TAU pathology in mouse models.

The paper shows that early-life caffeine exposure in Tau22 transgenic mice accelerates cognitive deficits linked to Alzheimer's-like pathology.

This study investigates the roles of endosomal-lysosomal and proteasomal pathways in processing APP-derived fragments, showing distinct degradation mechanisms for full-length APP and overexpressed C99.

This study shows that AMPK is essential for maintaining energy levels during synaptic activation by regulating mitochondrial respiration and supporting synaptic plasticity and memory formation.