{"entity": "journal", "iuid": "e91e8f8d558a48abab76afb6de13ab42", "timestamp": "2026-08-20T21:40:57.514Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/journal/Mov%20Disord.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/journal/Mov%20Disord"}}, "title": "Mov Disord", "issn": "1531-8257", "issn-l": null, "publications_count": 3, "publications": [{"entity": "publication", "iuid": "6a9ead4a969a405595755f49d3833c76", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/6a9ead4a969a405595755f49d3833c76.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/6a9ead4a969a405595755f49d3833c76"}}, "title": "Cerebrospinal Fluid Proteins Altered in Corticobasal Degeneration.", "authors": [{"family": "Paslawski", "given": "Wojciech", "initials": "W", "orcid": "0000-0003-2141-4547", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d9cd03bf75b24a37884524e605253073.json"}}, {"family": "Bergstr\u00f6m", "given": "Sofia", "initials": "S"}, {"family": "Zhang", "given": "Xiaoqun", "initials": "X"}, {"family": "Remnest\u00e5l", "given": "Julia", "initials": "J"}, {"family": "He", "given": "Yachao", "initials": "Y"}, {"family": "Boxer", "given": "Adam", "initials": "A"}, {"family": "M\u00e5nberg", "given": "Anna", "initials": "A"}, {"family": "Nilsson", "given": "Peter", "initials": "P"}, {"family": "Svenningsson", "given": "Per", "initials": "P"}], "type": "letter", "published": "2021-05-00", "journal": {"title": "Mov Disord", "issn": "1531-8257", "volume": "36", "issue": "5", "pages": "1278-1280", "issn-l": null}, "abstract": null, "doi": "10.1002/mds.28543", "pmid": "33660876", "labels": [], "xrefs": [], "notes": [], "created": "2026-08-20T06:34:26.485Z", "modified": "2026-08-20T06:34:26.573Z"}, {"entity": "publication", "iuid": "a213e2494b284b67858eebe80d6f46b0", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/a213e2494b284b67858eebe80d6f46b0.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/a213e2494b284b67858eebe80d6f46b0"}}, "title": "Involvement of Autophagy in Levodopa-Induced Dyskinesia.", "authors": [{"family": "Feyder", "given": "Michael", "initials": "M"}, {"family": "Plewnia", "given": "Carina", "initials": "C"}, {"family": "Lieberman", "given": "Ori J", "initials": "OJ"}, {"family": "Spigolon", "given": "Giada", "initials": "G"}, {"family": "Piccin", "given": "Alessandro", "initials": "A"}, {"family": "Urbina", "given": "Lidia", "initials": "L"}, {"family": "Dehay", "given": "Benjamin", "initials": "B", "orcid": "0000-0003-1723-9045", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/115cbf84637d4fc7805eb49404153129.json"}}, {"family": "Li", "given": "Qin", "initials": "Q"}, {"family": "Nilsson", "given": "Per", "initials": "P"}, {"family": "Altun", "given": "Mikael", "initials": "M"}, {"family": "Santini", "given": "Emanuela", "initials": "E"}, {"family": "Sulzer", "given": "David", "initials": "D", "orcid": "0000-0001-7632-0439", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/679638077d214a869041a2e5eaa0a784.json"}}, {"family": "Bezard", "given": "Erwan", "initials": "E"}, {"family": "Borgkvist", "given": "Anders", "initials": "A"}, {"family": "Fisone", "given": "Gilberto", "initials": "G", "orcid": "0000-0002-0719-8000", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1d33982666934283b42a11e51070951a.json"}}], "type": "journal article", "published": "2021-05-00", "journal": {"title": "Mov Disord", "issn": "1531-8257", "volume": "36", "issue": "5", "pages": "1137-1146", "issn-l": null}, "abstract": "Autophagy is intensively studied in cancer, metabolic and neurodegenerative diseases, but little is known about its role in pathological conditions linked to altered neurotransmission. We examined the involvement of autophagy in levodopa (l-dopa)-induced dyskinesia, a frequent motor complication developed in response to standard dopamine replacement therapy in parkinsonian patients.\n\nWe used mouse and non-human primate models of Parkinson's disease to examine changes in autophagy associated with chronic l-dopa administration and to establish a causative link between impaired autophagy and dyskinesia.\n\nWe found that l-dopa-induced dyskinesia is associated with accumulation of the autophagy-specific substrate p62, a marker of autophagy deficiency. Increased p62 was observed in a subset of projection neurons located in the striatum and depended on l-dopa-mediated activation of dopamine D1 receptors, and mammalian target of rapamycin. Inhibition of mammalian target of rapamycin complex 1 with rapamycin counteracted the impairment of autophagy produced by l-dopa, and reduced dyskinesia. The anti-dyskinetic effect of rapamycin was lost when autophagy was constitutively suppressed in D1 receptor-expressing striatal neurons, through inactivation of the autophagy-related gene protein 7.\n\nThese findings indicate that augmented responsiveness at D1 receptors leads to dysregulated autophagy, and results in the emergence of l-dopa-induced dyskinesia. They further suggest the enhancement of autophagy as a therapeutic strategy against dyskinesia. \u00a9 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.", "doi": "10.1002/mds.28480", "pmid": "33460487", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8248404"}], "notes": [], "created": "2026-08-20T06:34:24.631Z", "modified": "2026-08-20T06:34:24.789Z"}, {"entity": "publication", "iuid": "428654ddd32c4402a99e0ad2ce927267", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/428654ddd32c4402a99e0ad2ce927267.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/428654ddd32c4402a99e0ad2ce927267"}}, "title": "Cerebrospinal Fluid Levels of Kininogen-1 Indicate Early Cognitive Impairment in Parkinson's Disease.", "authors": [{"family": "Markaki", "given": "Ioanna", "initials": "I", "orcid": "0000-0003-3328-5746", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f31c405d780a4beeb64971dabd57cafd.json"}}, {"family": "Bergstr\u00f6m", "given": "Sofia", "initials": "S"}, {"family": "Tsitsi", "given": "Panagiota", "initials": "P"}, {"family": "Remnest\u00e5l", "given": "Julia", "initials": "J"}, {"family": "M\u00e5nberg", "given": "Anna", "initials": "A"}, {"family": "Hertz", "given": "Ellen", "initials": "E"}, {"family": "Paslawski", "given": "Wojciech", "initials": "W"}, {"family": "Sorjonen", "given": "Kimmo", "initials": "K"}, {"family": "Uhl\u00e9n", "given": "Mathias", "initials": "M"}, {"family": "Mangone", "given": "Graziella", "initials": "G"}, {"family": "Carvalho", "given": "Stephanie", "initials": "S"}, {"family": "Rascol", "given": "Olivier", "initials": "O"}, {"family": "Meissner", "given": "Wassilios G", "initials": "WG", "orcid": "0000-0003-2172-7527", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c37bb29c28fb49b6b5bd3e9a33a6aad6.json"}}, {"family": "Magnin", "given": "Eloi", "initials": "E"}, {"family": "W\u00fcllner", "given": "Ullrich", "initials": "U"}, {"family": "Corvol", "given": "Jean-Christophe", "initials": "JC"}, {"family": "Nilsson", "given": "Peter", "initials": "P"}, {"family": "Svenningsson", "given": "Per", "initials": "P"}], "type": "journal article", "published": "2020-11-00", "journal": {"title": "Mov Disord", "issn": "1531-8257", "volume": "35", "issue": "11", "pages": "2101-2106", "issn-l": null}, "abstract": "Cognitive impairment is common in patients with PD. Core markers of Alzheimer's dementia have been related also to PD dementia, but no disease-specific signature to predict PD dementia exists to date.\n\nThe aim of this study was to investigate CSF markers associated with cognition in early PD.\n\nA high-throughput suspension bead array examined 216 proteins in CSF of 74 PD patients in the AETIONOMY project. Cognitive function was assessed with Repeatable Battery for the Assessment of the Neuropsychological Status, Montreal Cognitive Assessment, and Mini-Mental State Examination.\n\nOf 69 patients with complete data, 34 had high (\u226590) and 35 had low Repeatable Battery for the Assessment of the Neuropsychological Status total score (<90). Of 14 proteins in CSF that differed in levels between groups, increased kininogen-1, validated with several antibodies, was independently associated with lower Repeatable Battery for the Assessment of the Neuropsychological Status and Montreal Cognitive Assessment scores after adjustment for confounders.\n\nKininogen-1 levels in CSF may serve as a marker of cognitive impairment in PD. \u00a9 2020 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.", "doi": "10.1002/mds.28192", "pmid": "33179332", "labels": [], "xrefs": [], "notes": [], "created": "2026-08-20T06:34:22.609Z", "modified": "2026-08-20T06:34:22.722Z"}], "created": "2026-08-20T06:34:22.688Z", "modified": "2026-08-20T06:34:22.688Z"}