iPSC QC (Adami et al, 2025)
By onSummary table and data from iPSC quality control experiments in Adami et al. 2025 are accessible for review.
Reply to: Is Gauchian genotyping of GBA1 variants reliable?
By onSummarizing a study by N. Tayebi et al. in Communications Biology, published in 2025.
Characterizing Parkinson’s Disease Clinical and Biomarker Interactions in REM Sleep Behavior Disorder
By ona-syn SAA positivity, DaT positivity, and hyposmia are highly associated with each other. MDS Prodromal PD Probability scores may be useful predictors of near-term progression, and thus as a stratification factor in clinical research study design
Inflamed Microglia like Macrophages in the Central Nervous System of Prodromal Parkinson′s Disease
By onWe investigated the role of inflammation in the pathogenesis of prodromal PD performing single-cell RNAseq analysis of CSF and blood from 111 individuals.
Article: PINK1 deficiency rewires early immune responses in a mouse model of Parkinson’s disease triggered by intestinal infection
By onPINK1 KO mice show PD-like symptoms post intestinal infections, with myeloid cells dysregulation and T cell response early after infection. PINK1 plays a key role in gut immune functions linked to early PD mechanisms.
Supporting data for “PINK1 deficiency rewires early immune responses in a mouse model of Parkinson’s disease triggered by intestinal infection”
By onData associated with “PINK1 deficiency rewires early immune responses in a mouse model of Parkinson’s disease triggered by intestinal infection”
Immunostaining and Western blot images
By onRaw immunostaining and western blot images included in Adami et al, 2025.
Baseline α–synuclein Seeding Activity and Disease Progression Code
By onThe project analyzes baseline α-synuclein seeding activity and Parkinson's disease progression.
Soluble Immune Factor Profiles in Blood and CSF Associated with LRRK2 Mutations and Parkinson’s Disease
By onThis preprint explores immune factors in Parkinson's disease linked to LRRK2 mutations. Serum showed elevated SDF-1 alpha and TNF-RII levels in LRRK2 carriers, while CSF had reduced immune markers. PD patients displayed reduced CSF inflammation.
Severe GBA1 variants drive the GBA-PD clinical phenotype: implications for counselling and clinical trials
By onVariants in the GBA1 gene are common genetic risk factors for Parkinson's disease. A study compared clinical phenotypes in GBA-PD and idiopathic PD patients, finding that only severe GBA-PD cases show a more severe clinical profile.
Exploring the relationship between GBA1 host genotype and gut microbiome in the GBA1L444P/WT mouse model: Implications for Parkinson disease pathogenesis
By onHeterozygous *GBA1* variants are common in Parkinson's disease. This study found no significant impact of the *GBA1* L444P variant on gut microbiome composition in mice, suggesting other factors may contribute to disease penetrance.
Immunohistochemistry (Brain organoids)
By onProtocol for preparing brain organoid slides and performing immunostainings to analyze protein expression and localization in the 3D model.
LINE-1 retrotransposons regulate the exit of human pluripotency and early brain development (Preprint)
By onHominoid-specific L1 retrotransposons are expressed in human stem cells and organoids. Silencing L1s leads to changes in neural differentiation and organoid size, suggesting L1 involvement in central nervous system development.
(x6) GBA heterozygous and homozygous mutant fibroblast lines available to share
By onCell lines deposited at ATCC used in a publication (10.1093/hmg/ddac233) include UCL-CTRL001, UCL-CTRL002, UCL-CTRL003, UCL-YCTRL001, UCL-E001K, UCL-N001S, and UCL-N002S, each with specific RRIDs.
Integrated multi-cohort analysis of the Parkinson’s disease gut metagenome
By onThe authors perform metagenomic sequencing of multiple geographically-disparate cohorts and find that stereotypic changes in the functional metabolic potential of the gut microbiome are a consistent feature of PD.
A prebiotic diet modulates microglial states and motor deficits in α-synuclein overexpressing mice
By onWhat should Parkinson's Disease patients eat? This study shows that dietary fiber impacts gut microbes and immune cells in the brain of a mouse model of Parkinson's.
R Code used in “Sex-Specific Microglial Responses to Glucocerebrosidase Inhibition: Relevance to GBA1-Linked Parkinson’s Disease”
By onR Code used in "sex-specific microglial responses to glucocerebrosidase inhibition: Relevance to GBA1-linked Parkinson’s disease."
Post-fibrillization nitration of alpha-synuclein abolishes its seeding activity and pathology formation in primary neurons and in vivo
By onIncreasing evidence points to post-translational modifications (PTMs) as key regulators of alpha-synuclein (α-Syn) function in health and disease. However, whether these PTMs occur before or after α-Syn pathology formation and their role in regulating α-Syn toxicity remain unclear. In this study, we demonstrate that post-fibrillization nitration of α-Syn fibrils induced their fragmentation, modified their surface and dynamic properties but not their structure, and nearly abolished their seeding activity in primary neurons and in vivo. Furthermore, we show that the dynamic and surface properties of the fibrils, rather than simply their length, are important determinants of α-Syn fibril seeding activity. Altogether, our work demonstrates that post-aggregation modifications of α-Syn may provide novel approaches to target a central process that contributes to pathology formation and disease progression. Finally, our results suggest that the pattern of PTMs on pathological aggregates, rather than simply their presence, could be a key determinant of their toxicity and neurodegeneration. This calls for reconsidering current approaches relying solely on quantifying and correlating the level of pathology to assess the efficacy of novel therapies, as not all α-Syn aggregates in the brain are pathogenic.
Indirect Proximity Ligation Assay (PLA) – Brightfield
By onThe authors describe the PLA protocol that is routinely used in the laboratory to detect nitrated alpha-synuclein and nitration of mitochondrial enzymes such as SOD2 and the mitochondrial complex 1 subunit NDUFB8.