Data files

Anti-amyloid β-peptide (Aβ) immunotherapy was developed as treatment for Alzheimer’s disease to reduce and prevent amyloid plaque pathology and its downstream consequences. Efficient amyloid plaque clearance has been proven in clinical trials with Aducanumab, Lecanemab and Donanemab. At least two of these antibodies slow memory decline to some extent and have beneficial effects on daily living activities. The therapeutic effects correlate with the efficacy of plaque removal. However, treatment ...

Despite numerous studies on fetal therapy for myelomeningoceles (MMC), the pathophysiology of this malformation remains poorly understood. This study aimed to analyze the biochemical profile and proteome of amniotic fluid (AF) supernatants from MMC fetuses to explore the prenatal pathophysiology. Proteome analysis was conducted in 18 MMC and 18 healthy singleton fetuses, as well as in 5 dichorionic pregnancies with MMC fetuses and their healthy co-twins. ELISA tests were used to validate proteome ...

Advancing MS-based proteomics towards clinical applications evolves around developing standardized start-to-finish and fit-for-purpose workflows for clinical specimens. Steps along the method design involve the determination and optimization of several bioanalytical parameters such as selectivity, sensitivity, accuracy, and precision. In a joint effort eight proteomics laboratories belonging to the MSCoreSys initiative including the CLINSPECT-M, MSTARS, DIASym, and SMART-CARE consortia performed ...

The cell surface receptor TREM2 is a key genetic risk factor and drug target in Alzheimer’s disease (AD). In the brain, TREM2 is expressed in microglia, where it undergoes proteolytic cleavage, linked to AD risk, but the responsible protease in microglia is unknown. Another microglia-expressed AD risk factor is inactive rhomboid 2 (iRhom2, RHBDF2), which acts as a non-catalytic subunit of the metalloprotease ADAM17. Its function in AD is unknown. To determine whether loss of iRhom2 and ADAM17 ...

The cell surface receptor TREM2 is a key genetic risk factor and drug target in Alzheimer’s disease (AD). In the brain, TREM2 is expressed in microglia, where it undergoes proteolytic cleavage, linked to AD risk, but the responsible protease in microglia is unknown. Another microglia-expressed AD risk factor is inactive rhomboid 2 (iRhom2, RHBDF2), which acts as a non-catalytic subunit of the metalloprotease ADAM17. Its function in AD is unknown. To determine whether loss of iRhom2 and ADAM17 ...

The beta-secretase beta-site APP cleaving enzyme 1 (BACE1) is a major drug target for Alzheimer’s disease (AD). Clinically tested BACE1 inhibitors induced unexpected cognitive side effects that may stem from their cross-inhibition of the homologous protease BACE2. Yet, little is known about BACE2 functions and substrates in vivo and no biomarker is available allowing to monitor the extent of BACE2 inhibition in vivo, in particular in cerebrospinal fluid (CSF). To identify a potential CSF biomarker ...

Quantitative mass spectrometry has transformed proteomics by allowing the simultaneous quantification of thousands of proteins. To boost statistical power, it is necessary to increase sample sizes by combining patient-derived data from various institutions. However, this practice raises significant privacy concerns. We created this dataset comtaining 30 healthy donors and 30 patients suffering from focal segmental glomerulosclerosis - a rare kidney disease - and distributed them to three independent ...