{"entity": "researcher", "timestamp": "2026-09-30T00:48:38.634Z", "family": "He", "given": "Yachao", "initials": "Y", "orcid": "0000-0002-0241-2901", "affiliations": ["Translational Neuropharmacology, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. yachao.he@ki.se."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/dda541fb10974d769b81a896c34c8947.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/dda541fb10974d769b81a896c34c8947"}}, "publications": [{"entity": "publication", "iuid": "45bf1d6bcca54873ab10a14c9742c11c", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/45bf1d6bcca54873ab10a14c9742c11c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/45bf1d6bcca54873ab10a14c9742c11c"}}, "title": "Prosaposin maintains lipid homeostasis in dopamine neurons and counteracts experimental parkinsonism in rodents.", "authors": [{"family": "He", "given": "Yachao", "initials": "Y", "orcid": "0000-0002-0241-2901", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/dda541fb10974d769b81a896c34c8947.json"}}, {"family": "Kaya", "given": "Ibrahim", "initials": "I", "orcid": "0000-0003-3345-5602", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/43885795cb254e2cba6fe8b538fbfaef.json"}}, {"family": "Shariatgorji", "given": "Reza", "initials": "R", "orcid": "0000-0001-9484-0921", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/76faa76e9dc445a3bbb1f470e9d33a23.json"}}, {"family": "Lundkvist", "given": "Johan", "initials": "J"}, {"family": "Wahlberg", "given": "Lars U", "initials": "LU"}, {"family": "Nilsson", "given": "Anna", "initials": "A"}, {"family": "Mamula", "given": "Dejan", "initials": "D"}, {"family": "Kehr", "given": "Jan", "initials": "J"}, {"family": "Zareba-Paslawska", "given": "Justyna", "initials": "J", "orcid": "0000-0001-6193-5908", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/966c469818f74df19b93d4a0d775182a.json"}}, {"family": "Biverst\u00e5l", "given": "Henrik", "initials": "H", "orcid": "0000-0002-2097-7658", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/603a87443b7b4315b6331a51e8103fb5.json"}}, {"family": "Chergui", "given": "Karima", "initials": "K"}, {"family": "Zhang", "given": "Xiaoqun", "initials": "X"}, {"family": "Andren", "given": "Per E", "initials": "PE", "orcid": "0000-0002-4062-7743", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f1dd27e8b238475383983480e10099f6.json"}}, {"family": "Svenningsson", "given": "Per", "initials": "P", "orcid": "0000-0001-6727-3802", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b01bbacfa24e4b9794734bf1121d1c38.json"}}], "type": "journal article", "published": "2023-09-19", "journal": {"title": "Nat Commun", "issn": "2041-1723", "volume": "14", "issue": "1", "pages": "5804", "issn-l": "2041-1723"}, "abstract": "Prosaposin (PSAP) modulates glycosphingolipid metabolism and variants have been linked to Parkinson's disease (PD). Here, we find altered PSAP levels in the plasma, CSF and post-mortem brain of PD patients. Altered plasma and CSF PSAP levels correlate with PD-related motor impairments. Dopaminergic PSAP-deficient (cPSAPDAT) mice display hypolocomotion and depression/anxiety-like symptoms with mildly impaired dopaminergic neurotransmission, while serotonergic PSAP-deficient (cPSAPSERT) mice behave normally. Spatial lipidomics revealed an accumulation of highly unsaturated and shortened lipids and reduction of sphingolipids throughout the brains of cPSAPDAT mice. The overexpression of \u03b1-synuclein via AAV lead to more severe dopaminergic degeneration and higher p-Ser129 \u03b1-synuclein levels in cPSAPDAT mice compared to WT mice. Overexpression of PSAP via AAV and encapsulated cell biodelivery protected against 6-OHDA and \u03b1-synuclein toxicity in wild-type rodents. Thus, these findings suggest PSAP may maintain dopaminergic lipid homeostasis, which is dysregulated in PD, and counteract experimental parkinsonism.", "doi": "10.1038/s41467-023-41539-5", "pmid": "37726325", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC10509278"}, {"db": "pii", "key": "10.1038/s41467-023-41539-5"}], "notes": [], "created": "2026-09-23T08:39:33.144Z", "modified": "2026-09-23T08:39:33.375Z"}, {"entity": "publication", "iuid": "1c5c56f9d7844c1f81c2cd9f5f432490", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/1c5c56f9d7844c1f81c2cd9f5f432490.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/1c5c56f9d7844c1f81c2cd9f5f432490"}}, "title": "Spatial lipidomics reveals brain region-specific changes of sulfatides in an experimental MPTP Parkinson's disease primate model.", "authors": [{"family": "Kaya", "given": "Ibrahim", "initials": "I"}, {"family": "Nilsson", "given": "Anna", "initials": "A"}, {"family": "Lupt\u00e1kov\u00e1", "given": "Dominika", "initials": "D", "orcid": "0000-0002-3691-2584", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5c4315e3e4b24bd2a889fa2c82d735a5.json"}}, {"family": "He", "given": "Yachao", "initials": "Y", "orcid": "0000-0002-0241-2901", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/dda541fb10974d769b81a896c34c8947.json"}}, {"family": "Vallianatou", "given": "Theodosia", "initials": "T", "orcid": "0000-0002-1477-7756", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4374524ab2c14bd9ae46f904144dea63.json"}}, {"family": "Bj\u00e4rterot", "given": "Patrik", "initials": "P", "orcid": "0000-0002-4350-5530", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0a958cde39e9471881c0282f9d62f39c.json"}}, {"family": "Svenningsson", "given": "Per", "initials": "P", "orcid": "0000-0001-6727-3802", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b01bbacfa24e4b9794734bf1121d1c38.json"}}, {"family": "Bezard", "given": "Erwan", "initials": "E", "orcid": "0000-0002-0410-4638", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/92f25ac8ff1d46ce8b68fbd88cd36843.json"}}, {"family": "Andr\u00e9n", "given": "Per E", "initials": "PE", "orcid": "0000-0002-4062-7743", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f1dd27e8b238475383983480e10099f6.json"}}], "type": "journal article", "published": "2023-07-26", "journal": {"title": "NPJ Parkinsons Dis", "issn": "2373-8057", "volume": "9", "issue": "1", "pages": "118", "issn-l": null}, "abstract": "Metabolism of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) to the neurotoxin MPP+ in the brain causes permanent Parkinson's disease-like symptoms by destroying dopaminergic neurons in the pars compacta of the substantia nigra in humans and non-human primates. However, the complete molecular pathology underlying MPTP-induced parkinsonism remains poorly understood. We used dual polarity matrix-assisted laser desorption/ionization mass spectrometry imaging to thoroughly image numerous glycerophospholipids and sphingolipids in coronal brain tissue sections of MPTP-lesioned and control non-human primate brains (Macaca mulatta). The results revealed specific distributions of several sulfatide lipid molecules based on chain-length, number of double bonds, and importantly, hydroxylation stage. More specifically, certain long-chain hydroxylated sulfatides with polyunsaturated chains in the molecular structure were depleted within motor-related brain regions in the MPTP-lesioned animals, e.g., external and internal segments of globus pallidus and substantia nigra pars reticulata. In contrast, certain long-chain non-hydroxylated sulfatides were found to be elevated within the same brain regions. These findings demonstrate region-specific dysregulation of sulfatide metabolism within the MPTP-lesioned macaque brain. The depletion of long-chain hydroxylated sulfatides in the MPTP-induced pathology indicates oxidative stress and oligodendrocyte/myelin damage within the pathologically relevant brain regions. Hence, the presented findings improve our current understanding of the molecular pathology of MPTP-induced parkinsonism within primate brains, and provide a basis for further research regarding the role of dysregulated sulfatide metabolism in PD.", "doi": "10.1038/s41531-023-00558-1", "pmid": "37495571", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC10372136"}, {"db": "pii", "key": "10.1038/s41531-023-00558-1"}], "notes": [], "created": "2026-09-23T08:45:57.678Z", "modified": "2026-09-23T08:45:57.833Z"}]}