Joanna Bons

This study shows that oral DBM treatment prevents cognitive decline in a C9ORF72 FTD mouse model without altering protein inclusions but corrects gene expression changes related to cytoskeleton, ALS, and metabolism.

This paper develops a proteomic workflow to confidently identify and quantify lysine methylmalonylation in mouse brain tissue, revealing its regulation by SIRT5 and its role in myelin stability.

This study shows APOE4 affects female bone quality more than male bone, without structural changes, by disrupting osteocyte function.

This study uses PAMAF mode HRIM-MS to quantify succinylation sites in mouse kidney, showing Sirt5 regulates succinylation of mitochondrial proteins involved in metabolism.

This study uses spatial mass spectrometry imaging to identify ECM peptide markers distinguishing OA-affected subchondral bone from healthy tissue and less affected regions.

This study shows that overexpressing an Alu transposon in human fibroblasts causes widespread disruptions in aging-related pathways across transcriptome, proteome, and secretome.

This study shows that feeding mice odd-chain dicarboxylic acids reproduces the biochemical features of glutaric aciduria type-1.

This paper develops a proteomic workflow using data-independent acquisitions to analyze APOE3-derived neurons and microglia, identifying cell type-specific markers and pathways.

This study identifies aging-associated proteomic and lipid signatures in exosomes from senescent cells and human plasma, revealing shared biomarkers and pathways linked to senescence and tissue damage.

The paper identifies a fibroblast state called STIF that drives YAP-dependent regenerative programs and (pre)malignancy through mechanotransduction in response to tissue injury.

This study identifies age-related dysregulation of the splicing machinery in older AML patients through proteomic analysis, highlighting potential targets for age-specific therapies.

The paper establishes a senotype of doxorubicin-induced senescence in postmenopausal human ovarian tissue using single nuclei sequencing and proteomics.

The paper introduces iprm-PASEF, a targeted MSI method, to identify and quantify metabolites and lipids in CD38 knockout mice, showing increased NAD+ and decreased ADPR.

This study identifies Sirt5's role in regulating chondrocyte metabolism and osteoarthritis through lysine malonylation, showing its dysregulation contributes to OA in aging and obesity.

This study identifies ADAM19 as a modulator of the senescence-associated secretory phenotype (SASP) and shows that its inhibition reduces gut permeability and senescence markers in multiple species.

This study shows that loss of LCAD protects against acute kidney injury by reducing oxidative stress and enhancing peroxisomal fatty acid oxidation.

The paper identifies stromal protein profiles in breast cancer subtypes using proteomic analysis of FFPE tissues, revealing significant ECM and immune-related changes, particularly in metaplastic breast cancer.

This study shows that substrate stiffness influences doxorubicin-induced senescence and secretory profiles in human pulmonary fibroblasts, with collagen enrichment observed in high-stiffness conditions.

This study shows that deleting TYROBP in HD mice reduces microglial activation and improves motor deficits without correcting neuronal gene expression.

This study identifies high stoichiometry lysine succinylation sites in mouse liver, showing their functional role in urea cycle regulation and ammonia metabolism through SIRT5.

This study shows that a short-term cyclic ketogenic diet improves memory and synaptic plasticity in aged mice by modulating the cAMP/PKA signaling pathway and cytoskeleton dynamics.

The paper performs proteomic analysis of Huntington's disease patient-derived medium spiny neurons, identifying altered lipid metabolism and lipid droplet accumulation as key findings.

The paper identifies SIRT5 and KAT2A as regulators of histone malonylation, showing its role in ribosomal gene expression and age-related changes in mouse brains.

This study shows that fructose metabolism via KHK-C increases ER stress and modulates the hepatic transcriptome, contributing to NAFLD progression in both genetic and diet-induced models.

This study shows that senescent Schwann cells, induced by aging and chronic denervation, impair axonal regeneration by reducing c-Jun expression and secreting inhibitory factors, and that eliminating these cells improves regeneration.