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Keuren-Jensen, K. V.

Publications and source records attributed to Keuren-Jensen, K. V..

3 recordsLinked to original sources

Profiling of Aggregated Amyloid β42-induced Proteomic Alterations in KOLF2.1J Induced Pluripotent Stem Cell-derived Neurons

Amyloid[beta]; (A[beta];) plaques are a hallmark of Alzheimer[prime]s disease (AD). A human cellular neuronal model that recaptures A[beta];-induced pathology is critical for advancing AD research. However, comprehensive proteomic profiling of A[beta];-induced cellular model remains elusive. In this study, we investigated the proteomic changes in induced pluripotent stem cell (iPSC)-derived neurons (iNs) exposed to synthetic A[beta]; (1-42) peptides (A[beta];42A) to improve our understanding of the cellular responses of A[beta]; aggregates and to establish a human-related platform for AD research. A[beta];42A formed extracellular aggregates around neuronal soma and neurites, impaired neurite outgrowth, and induced the expression of multiple AD-associated genes, such as APOE, BACE1, ADAM10. To define the molecular landscape of A[beta];-induced neuronal dysfunction, we performed proteomic analyses of whole-cell lysates as well as soma- and neurite-enriched fractions. Proteomic profiling revealed extensive gene alterations in pathways associated with synaptic function, neuronal maintenance, and AD pathogenesis, such as the upregulation of APOE. Importantly, the A[beta];42A-iNs system recapitulated molecular signatures observed in AD brain tissue and cerebrospinal fluid. Representative protein changes, including APOE upregulation and its colocalization with A[beta]; aggregates, were further validated in postmortem human AD brain tissue. Together, these findings manifest that the A[beta];42A-iNs system reproduces multiple cellular and molecular features of AD and exhibits strongly consensus with clinical observations. It provides a valuable platform for investigating A[beta];-driven neurodegeneration and for the discovery of therapeutic targets for AD.

neuroscience↗

Large-scale HLA immunopeptidome and interactome profiling in microglia

Microglia are immune cells of the brain and act as major antigen presenting cells. Antigen presentation involves the human leukocyte antigen (HLA) complex, which is implicated in genetic risk of multiple neurodegenerative diseases. How HLA affects the function of microglia in the context of neurodegenerative disease remains unclear. Here, we investigated the HLA epitopes and their protein interactome in human induced pluripotent stem cell (iPSC)-derived microglia-like cells (iMGLs) using systematic mass spectrometry (MS)-based immunopeptidomics, whole-cell proteomics, affinity purification, and prediction algorithms. Our results revealed the presence of almost 7,000 peptides presented by HLA class I and II within microglia. We further showed that the immunopeptidome landscapes of iPSCs, iMGLs and interferon-gamma (IFN{gamma}) stimulated iMGLs are all readily distinguishable. Furthermore, HLA interacts with different groups of proteins in iPSCs compared to iMGLs which involve proteins in immune response. Importantly, we detected 25 HLA epitopes derived from 15 genes associated with Alzheimers and related dementias such as Tau, PLD3 (Alzheimers disease), TDP-43, FUS (Frontotemporal dementia), and PARK7, VPS35 (Lewy Body dementia). We predicted 31 mutant epitopes derived from these ADRD genes that could be presented with strong interaction to HLA molecules. Along with these epitopes, we observed an enrichment of immune-related interaction proteins in microglia treated with IFN{gamma}. These results provide evidence that aggregated and mutated proteins can interact with HLA alleles and be presented on the cell surface by microglia cells. This study sheds light on the antigen presenting and adaptive immunity mechanism within the central nervous system and its possible effects on neurodegenerative diseases.

immunology↗

Multi-Modality Machine Learning Predicting Parkinsons Disease

BackgroundPersonalized medicine promises individualized disease prediction and treatment. The convergence of machine learning (ML) and available multi-modal data is key moving forward. We build upon previous work to deliver multi-modal predictions of Parkinsons Disease (PD). MethodsWe performed automated ML on multi-modal data from the Parkinsons Progression Marker Initiative (PPMI). After selecting the best performing algorithm, all PPMI data was used to tune the selected model. The model was validated in the Parkinsons Disease Biomarker Program (PDBP) dataset. Finally, networks were built to identify gene communities specific to PD. FindingsOur initial model showed an area under the curve (AUC) of 89.72% for the diagnosis of PD. The tuned model was then tested for validation on external data (PDBP, AUC 85.03%). Optimizing thresholds for classification, increased the diagnosis prediction accuracy (balanced accuracy) and other metrics. Combining data modalities outperforms the single biomarker paradigm. UPSIT was the largest contributing predictor for the classification of PD. The transcriptomic data was used to construct a network of disease-relevant transcripts. InterpretationWe have built a model using an automated ML pipeline to make improved multi-omic predictions of PD. The model developed improves disease risk prediction, a critical step for better assessment of PD risk. We constructed gene expression networks for the next generation of genomics-derived interventions. Our automated ML approach allows complex predictive models to be reproducible and accessible to the community. FundingNational Institute on Aging, National Institute of Neurological Disorders and Stroke, the Michael J. Fox Foundation, and the Global Parkinsons Genetics Program. RESEARCH IN CONTEXTO_ST_ABSEvidence before this studyC_ST_ABSPrior research into predictors of Parkinsons disease (PD) has either used basic statistical methods to make predictions across data modalities, or they have focused on a single data type or biomarker model. We have done this using an open-source automated machine learning (ML) framework on extensive multi-modal data, which we believe yields robust and reproducible results. We consider this the first true multi-modality ML study of PD risk classification. Added value of this studyWe used a variety of linear, non-linear, kernel, neural networks, and ensemble ML algorithms to generate an accurate classification of both cases and controls in independent datasets using data that is not involved in PD diagnosis itself at study recruitment. The model built in this paper significantly improves upon our previous models that used the entire training dataset in previous work1. Building on this earlier work, we showed that the PD diagnosis can be refined using improved algorithmic classification tools that may yield potential biological insights. We have taken careful consideration to develop and validate this model using public controlled-access datasets and an open-source ML framework to allow for reproducible and transparent results. Implications of all available evidenceTraining, validating, and tuning a diagnostic algorithm for PD will allow us to augment clinical diagnoses or risk assessments with less need for complex and expensive exams. Going forward, these models can be built on remote or asynchronously collected data which may be important in a growing telemedicine paradigm. More refined diagnostics will also increase clinical trial efficiency by potentially refining phenotyping and predicting onset, allowing providers to identify potential cases earlier. Early detection could lead to improved treatment response and higher efficacy. Finally, as part of our workflow, we built new networks representing communities of genes correlated in PD cases in a hypothesis-free manner, showing how new and existing genes may be connected and highlighting therapeutic opportunities.

genomics↗