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Athieniti, E.

Publications and source records attributed to Athieniti, E..

2 recordsLinked to original sources

Multi-omics dissection of Parkinson's patient subgroups associated with motor and cognitive severity

Heterogeneity in the severity of Parkinsons disease (PD) inhibits the effective interpretation of clinical trial outcomes. Multi-omics analysis may help explain the pathological mechanisms underlying disease progression and reveal biomarkers of clinical severity. We performed Multi-Omics Factor Analysis (MOFA) on whole blood RNA, miRNA and Cerebrospinal fluid (CSF) and blood plasma proteomics from the Parkinsons Progression Marker Initiative (PPMI), to identify molecular factors correlated with motor (MDS-UPDRS3) and cognitive (Semantic Fluency Test, SFT) function. Three molecular factors significantly correlated with the MDS-UPDRS3 score and two with SFT, which remained significant after adjusting for age, sex, and medication dose. We used the identified factors to stratify patients into subgroups with distinct motor and cognitive severity. The severe motor clusters showed deregulation of cytotoxic natural killer cell mechanisms in peripheral blood, and changes to proteins associated with the endoplasmic reticulum in CSF. The severe cognitive clusters showed changes in complement and synaptic dysfunction. Our analysis capitalizes on multi-omics data integration to enrich our understanding of the mechanisms driving motor and cognitive decline in PD, to support precision medicine.

bioinformatics↗

Stage-specific gene ratios highlight genes and mechanisms related to presymptomatic and symptomatic Multiple Myeloma

Background/aimMultiple Myeloma is the second most common blood cancer, characterised by the accumulation of malignant plasma cells and the production of large amounts of a monoclonal immunoglobulin protein, in the bone marrow. The identification and progression/behaviour of molecular markers across stages remains a scientific challenge. This work aims to provide a holistic approach to the understanding of the disease progression, providing specific methodologies and candidate biomarkers, able to characterise and distinguish the disease state across stages. Materials and methodsTwo large bulk RNA datasets were used to collect and integrate stage-specific information at the gene level by means of: (a) differential expression analysis to obtain differential expressed genes (DEGs), (b) a recently introduced computational methodology able to detect monotonically expressed genes (MEGs), (c) a proposed computational methodology that uses pairs of MEGs at sample level, to classify and discriminate different stages of Multiple Myeloma. Additional numerical metrics were applied to rank the performance of these pairs across samples, facilitating the characterization and differentiation of disease stages. Validation was conducted using five additional external datasets, which were then utilised to enrich the final selection of top-rated genes identified from the two bulk RNA datasets under study. The final top-ranked genes were further used for pathway enrichment analysis in order to provide candidate pathways per stage. ResultsWe first show that MEGs provide better statistics than DEGs, both at gene and pathway level analysis. Secondly, we show that the proposed computational methodology by means of MEGs reveals short lists of high discriminative genes across stages, which in turn highlight significant groups of pathways. ConclusionWe integrated traditional analysis of DEGs with a recently introduced methodology for identifying MEGs, creating a novel computational approach capable of identifying highly discriminative genes and pathways that can serve as candidate markers for stage identification in a single sample. HighlightsO_LIA novel computational approach was used to identify Monotonically Expressed Genes (MEGs) whose expression was constantly increasing or decreasing. Genes such as RB1, CD27, TP53, and MCL1, previously highlighted in Multiple Myeloma, showed a consistent monotonic pattern, providing potential indicators for tracking the progression from the pre-malignant stages to active Multiple Myeloma. C_LIO_LIThe study calculated gene pair ratios using MEGs characterised by normal distribution and low dispersion. These ratios effectively distinguished healthy from disease samples, although the discrimination between disease stages (MGUS, SMM, MM) was less clear due to their overlapping molecular profiles. C_LIO_LIEnrichment analysis of significant gene pairs identified critical pathways affected during Multiple Myeloma progression, such as bone disease-related calcium pathways, glucocorticoid-regulated functions, and cardiac and neurological systems. These findings align with known clinical manifestations in MM patients, such as bone disease and amyloid cardiomyopathy. C_LIO_LIThe gene lists generated from our computational approach were validated against internal and external datasets, confirming their applicability. The methodology showed promise in identifying candidate genes for disease progression and could be applied to other diseases to uncover novel gene pairs not highlighted by traditional analyses. C_LI

bioinformatics↗