371 - 380 of 7939 Results
Title
Year
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OPENTitle: Common genetic risk for Parkinson's disease and dysfunction of the endo-lysosomal systemJournal Name: Philosophical Transactions of the Royal Society B: Biological SciencesPublisher: The Royal SocietyVol: 379Issue #: 1899Start Page:End Page:Publication Date:Open Access(OA) Status: OPENLicense: cc-by, cc-byDOI - Digital Object Identifier: 10.1098/rstb.2022.0517Citation Count: 3
- Data‐driven disease progression model of Parkinson's disease and effect of sex and genetic variants2024OPENTitle: Data‐driven disease progression model of Parkinson's disease and effect of sex and genetic variantsJournal Name: CPT: Pharmacometrics & Systems PharmacologyPublisher: WileyVol: 13Issue #: 4Start Page: 649End Page: 659Publication Date:Open Access(OA) Status: OPENLicense: cc-by-ncDOI - Digital Object Identifier: 10.1002/psp4.13112Citation Count: 2
- Endo-lysosomal dysfunction in neurodegenerative diseases: opinion on current progress and future direction in the use of exosomes as biomarkers2024RESTRICTEDTitle: Endo-lysosomal dysfunction in neurodegenerative diseases: opinion on current progress and future direction in the use of exosomes as biomarkersJournal Name: Philosophical Transactions of the Royal Society B: Biological SciencesPublisher: The Royal SocietyVol: 379Issue #: 1899Start Page:End Page:Publication Date:Open Access(OA) Status: RESTRICTEDLicense: cc-byDOI - Digital Object Identifier: 10.1098/rstb.2022.0387Citation Count: 3
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OPENTitle: Retromer-dependent lysosomal stress in Parkinson's diseaseJournal Name: Philosophical Transactions of the Royal Society B: Biological SciencesPublisher: The Royal SocietyVol: 379Issue #: 1899Start Page:End Page:Publication Date:Open Access(OA) Status: OPENLicense: cc-byDOI - Digital Object Identifier: 10.1098/rstb.2022.0376Citation Count: 2
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OPENTitle: Role of the LRRK2 C-terminal tail in domain crosstalkJournal Name: Biochemical JournalPublisher: Portland Press Ltd.Vol: 481Issue #: 4Start Page: 313End Page: 327Publication Date:Open Access(OA) Status: OPENLicense: cc-byDOI - Digital Object Identifier: 10.1042/bcj20230477Citation Count: 0
- Common mitochondrial deletions in RNA-Seq: evaluation of bulk, single-cell, and spatial transcriptomic datasets2024OPENTitle: Common mitochondrial deletions in RNA-Seq: evaluation of bulk, single-cell, and spatial transcriptomic datasetsJournal Name: Communications BiologyPublisher: Springer Science and Business Media LLCVol: 7Issue #: 1Start Page:End Page:Publication Date:Open Access(OA) Status: OPENLicense: cc-byDOI - Digital Object Identifier: 10.1038/s42003-024-05877-4Citation Count: 1
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OPENTitle: Levodopa Impairs the Energy Metabolism of the Basal Ganglia In VivoJournal Name: Annals of NeurologyPublisher: WileyVol: 95Issue #: 5Start Page: 849End Page: 857Publication Date:Open Access(OA) Status: OPENLicense: cc-by-nc-ndDOI - Digital Object Identifier: 10.1002/ana.26884Citation Count: 3
- Pathogenetic Contributions and Therapeutic Implications of Transglutaminase 2 in Neurodegenerative Diseases2024OPENTitle: Pathogenetic Contributions and Therapeutic Implications of Transglutaminase 2 in Neurodegenerative DiseasesJournal Name: International Journal of Molecular SciencesPublisher: MDPI AGVol: 25Issue #: 4Start Page: 2364End Page: 2364Publication Date:Open Access(OA) Status: OPENLicense: cc-byDOI - Digital Object Identifier: 10.3390/ijms25042364Citation Count: 1
- Multi-cohort cerebrospinal fluid proteomics identifies robust molecular signatures for asymptomatic and symptomatic Alzheimer’s disease.2024OPENTitle: Multi-cohort cerebrospinal fluid proteomics identifies robust molecular signatures for asymptomatic and symptomatic Alzheimer’s disease.Journal Name:Publisher: Research Square Platform LLCVol:Issue #:Start Page:End Page:Publication Date:Open Access(OA) Status: OPENLicense:DOI - Digital Object Identifier: 10.21203/rs.3.rs-3631708/v1Citation Count: 0
- Reduced progranulin increases tau and α-synuclein inclusions and alters mouse tauopathy phenotypes via glucocerebrosidase2024OPENTitle: Reduced progranulin increases tau and α-synuclein inclusions and alters mouse tauopathy phenotypes via glucocerebrosidaseJournal Name: Nature CommunicationsPublisher: Springer Science and Business Media LLCVol: 15Issue #: 1Start Page:End Page:Publication Date:Open Access(OA) Status: OPENLicense: cc-byDOI - Digital Object Identifier: 10.1038/s41467-024-45692-3Best OA location URL: https://doi.org/10.1038/s41467-024-45692-3Citation Count: 1