{"entity": "researcher", "timestamp": "2026-07-20T22:03:48.504Z", "family": "Jackson", "given": "Walker S", "initials": "WS", "orcid": "0000-0002-3003-5509", "affiliations": ["Department of Biomedical and Clinical Sciences, Wallenberg Center for Molecular Medicine, Link\u00f6ping University, Link\u00f6ping, Sweden walker.jackson@liu.se.", "German Center for Neurodegenerative Diseases, Bonn, Germany."], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/62f49c7978954d098514c5b1bfa9e34b.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/62f49c7978954d098514c5b1bfa9e34b"}}, "publications": [{"entity": "publication", "iuid": "e7038b6561ed4a8282747388827a8dac", "links": {"self": {"href": "https://publications.scilifelab.se/publication/e7038b6561ed4a8282747388827a8dac.json"}, "display": {"href": "https://publications.scilifelab.se/publication/e7038b6561ed4a8282747388827a8dac"}}, "title": "Neuroinflammation and neurodegeneration trigger a specific splice form of ribosomal protein S24", "authors": [{"family": "Magadi", "given": "Srivathsa S", "initials": "SS"}, {"family": "Jonson", "given": "Maria", "initials": "M"}, {"family": "Lucena", "given": "Pablo B", "initials": "PB"}, {"family": "Caliandro", "given": "Michele F", "initials": "MF"}, {"family": "Almeida", "given": "Beatriz", "initials": "B"}, {"family": "Bilalli", "given": "Lorina", "initials": "L"}, {"family": "Budinger", "given": "Dimitri", "initials": "D", "orcid": "0000-0001-7002-1091", "researcher": {"href": "https://publications.scilifelab.se/researcher/ecc1d3189e714b89a58b392e2a05eb8e.json"}}, {"family": "Tsoi", "given": "Anna", "initials": "A"}, {"family": "Ntzouni", "given": "Maria", "initials": "M"}, {"family": "Maqdissi", "given": "Joseph Agi", "initials": "JA"}, {"family": "Kaczmarczyk", "given": "Lech", "initials": "L", "orcid": "0000-0003-2747-3134", "researcher": {"href": "https://publications.scilifelab.se/researcher/2b192685d0c2438497741e66bfc183c9.json"}}, {"family": "Zijlstra", "given": "Jente J", "initials": "JJ"}, {"family": "Faketija", "given": "Matej", "initials": "M"}, {"family": "Perkins", "given": "Matthew", "initials": "M"}, {"family": "Paul", "given": "Gesine", "initials": "G", "orcid": "0000-0002-6806-2254", "researcher": {"href": "https://publications.scilifelab.se/researcher/dbbb29ff13af4e28afddbf78764cad29.json"}}, {"family": "Hallbeck", "given": "Martin", "initials": "M", "orcid": "0000-0001-6716-0314", "researcher": {"href": "https://publications.scilifelab.se/researcher/17f7b361871045a1b1e3cdfec9ebe5ec.json"}}, {"family": "Ingelsson", "given": "Martin", "initials": "M", "orcid": "0000-0001-5466-8370", "researcher": {"href": "https://publications.scilifelab.se/researcher/903a14004e794693bebb8c8ca345c626.json"}}, {"family": "Watts", "given": "Joel C", "initials": "JC"}, {"family": "Reichenbach", "given": "Nicole", "initials": "N"}, {"family": "Petzold", "given": "Gabor C", "initials": "GC", "orcid": "0000-0002-0145-8641", "researcher": {"href": "https://publications.scilifelab.se/researcher/0a64d37850384e10a8a4199ea81ae856.json"}}, {"family": "Schieweck", "given": "Rico", "initials": "R"}, {"family": "Heneka", "given": "Michael T", "initials": "MT", "orcid": "0000-0003-4996-1630", "researcher": {"href": "https://publications.scilifelab.se/researcher/8c46f161bc8544a78eef05ee0b74bb47.json"}}, {"family": "Jackson", "given": "Walker S", "initials": "WS", "orcid": "0000-0002-3003-5509", "researcher": {"href": "https://publications.scilifelab.se/researcher/62f49c7978954d098514c5b1bfa9e34b.json"}}], "type": "journal-article", "published": "2026-05-06", "journal": {"title": "Brain", "issn": "0006-8950", "issn-l": null}, "abstract": "Neuroinflammation, particularly that involving reactive microglia, the brain's resident immune cells, is implicated in the pathogenesis of major neurodegenerative diseases (NDs). Multiple studies have reported changes in ribosomal protein (RP) expression during neurodegeneration, but the significance of these changes remains unclear. Ribosomes are evolutionarily conserved protein-synthesizing machines, and although commonly viewed as invariant, accumulating evidence suggests functional ribosome specialization through variation in their protein composition. Among RPs, S24, encoded by RPS24 in humans and Rps24 in mice, is unique as its transcripts undergo alternative splicing to produce protein variants with different C-terminal sequences that are differentially expressed across tissues and cell types. Understanding heterogeneous RP expression patterns across brain regions and cell types could reveal mechanisms underlying selective vulnerability in NDs and provide new biomarkers for neuroinflammatory responses. To identify RP expression patterns across brain regions in neurons, astrocytes, and microglia we analyzed cell type-specific translating mRNAs from mice. To investigate Rps24 isoform-specific expression, we performed cell type-resolved transcript analysis and developed antibodies specific for the S24-PKE protein variant encoded by mRNA isoform Rps24c. We examined Rps24c/S24-PKE expression in brains from mouse models of aging and neurodegeneration, as well as in human postmortem tissue from patients with Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). This work revealed distinct RP expression patterns across brain regions and between neurons, astrocytes, and microglia, including neuron-enriched RPs Rpl13a and Rps10. Analysis of RP paralogs revealed complex expression relationships with their canonical counterparts, suggesting regulated mechanisms for generating heterogeneous ribosomes. Across brain regions and cell types, Rplp0 and Rpl13a, commonly used normalization references, showed heterogeneous expression, raising important methodological considerations for gene expression studies. Rps24 isoforms exhibited striking cell type-specific expression patterns. Rps24c was predominantly expressed in microglia and was increased by neuroinflammation caused by aging, neurodegeneration, or inflammatory chemicals. Using S24-PKE-specific antibodies, we verified increased expression of this protein variant in brains with AD, PD, and HD, and in relevant mouse models. These findings establish heterogeneous RP expression as a feature of brain cell types which may enable cell type-specific translation regulation via specialized ribosomes. This work also identifies Rps24c/S24-PKE as a potential novel marker for neuroinflammation and neurodegeneration and provides new tools for monitoring these responses.", "doi": "10.1093/brain/awag166", "pmid": "42087813", "labels": {"NGI Short read": "Service", "NGI Stockholm (Genomics Production)": "Service", "National Genomics Infrastructure": "Service"}, "xrefs": [{"db": "pii", "key": "8670210"}], "notes": [], "created": "2026-05-11T12:23:19.422Z", "modified": "2026-07-10T08:27:01.238Z"}, {"entity": "publication", "iuid": "818ae71d23b34d728f0d3eb5a1db3dde", "links": {"self": {"href": "https://publications.scilifelab.se/publication/818ae71d23b34d728f0d3eb5a1db3dde.json"}, "display": {"href": "https://publications.scilifelab.se/publication/818ae71d23b34d728f0d3eb5a1db3dde"}}, "title": "Cerebellar granule neurons induce Cyclin D1 before the onset of motor symptoms in Huntington's disease mice.", "authors": [{"family": "Bauer", "given": "Susanne", "initials": "S"}, {"family": "Chen", "given": "Chwen-Yu", "initials": "CY"}, {"family": "Jonson", "given": "Maria", "initials": "M"}, {"family": "Kaczmarczyk", "given": "Lech", "initials": "L"}, {"family": "Magadi", "given": "Srivathsa Subramanya", "initials": "SS"}, {"family": "Jackson", "given": "Walker S", "initials": "WS", "orcid": "0000-0002-3003-5509", "researcher": {"href": "https://publications.scilifelab.se/researcher/62f49c7978954d098514c5b1bfa9e34b.json"}}], "type": "journal article", "published": "2023-01-20", "journal": {"title": "Acta Neuropathol Commun", "issn": "2051-5960", "volume": "11", "issue": "1", "pages": "17", "issn-l": "2051-5960"}, "abstract": "Although Huntington's disease (HD) is classically defined by the selective vulnerability of striatal projection neurons, there is increasing evidence that cerebellar degeneration modulates clinical symptoms. However, little is known about cell type-specific responses of cerebellar neurons in HD. To dissect early disease mechanisms in the cerebellum and cerebrum, we analyzed translatomes of neuronal cell types from both regions in a new HD mouse model. For this, HdhQ200 knock-in mice were backcrossed with the calm 129S4 strain, to constrain experimental noise caused by variable hyperactivity of mice in a C57BL/6 background. Behavioral and neuropathological characterization showed that these S4-HdhQ200 mice had very mild behavioral abnormalities starting around 12 months of age that remained mild up to 18 months. By 9 months, we observed abundant Huntingtin-positive neuronal intranuclear inclusions (NIIs) in the striatum and cerebellum. The translatome analysis of GABAergic cells of the cerebrum further confirmed changes typical of HD-induced striatal pathology. Surprisingly, we observed the strongest response with 626 differentially expressed genes in glutamatergic neurons of the cerebellum, a population consisting primarily of granule cells, commonly considered disease resistant. Our findings suggest vesicular fusion and exocytosis, as well as differentiation-related pathways are affected in these neurons. Furthermore, increased expression of cyclin D1 (Ccnd1) in the granular layer and upregulated expression of polycomb group complex protein genes and cell cycle regulators Cbx2, Cbx4 and Cbx8 point to a putative role of aberrant cell cycle regulation in cerebellar granule cells in early disease.", "doi": "10.1186/s40478-022-01500-x", "pmid": "36670467", "labels": {"Bioinformatics Support and Infrastructure": "Service", "Bioinformatics Support, Infrastructure and Training": "Service", "Bioinformatics Support for Computational Resources": "Service", "Bioinformatics (NBIS)": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC9854201"}, {"db": "pii", "key": "10.1186/s40478-022-01500-x"}], "notes": [], "created": "2023-12-01T13:21:09.700Z", "modified": "2024-01-16T13:48:34.107Z"}, {"entity": "publication", "iuid": "db2cb53665f444ec82e2dad906899885", "links": {"self": {"href": "https://publications.scilifelab.se/publication/db2cb53665f444ec82e2dad906899885.json"}, "display": {"href": "https://publications.scilifelab.se/publication/db2cb53665f444ec82e2dad906899885"}}, "title": "Translatome profiling in fatal familial insomnia implicates TOR signaling in somatostatin neurons.", "authors": [{"family": "Bauer", "given": "Susanne", "initials": "S", "orcid": "0000-0003-4731-5002", "researcher": {"href": "https://publications.scilifelab.se/researcher/6b6d3b8355fa4f41b7015a8ffe8f398c.json"}}, {"family": "Dittrich", "given": "Lars", "initials": "L"}, {"family": "Kaczmarczyk", "given": "Lech", "initials": "L", "orcid": "0000-0003-2747-3134", "researcher": {"href": "https://publications.scilifelab.se/researcher/2b192685d0c2438497741e66bfc183c9.json"}}, {"family": "Schleif", "given": "Melvin", "initials": "M"}, {"family": "Benfeitas", "given": "Rui", "initials": "R"}, {"family": "Jackson", "given": "Walker S", "initials": "WS", "orcid": "0000-0002-3003-5509", "researcher": {"href": "https://publications.scilifelab.se/researcher/62f49c7978954d098514c5b1bfa9e34b.json"}}], "type": "journal article", "published": "2022-11-00", "journal": {"title": "Life Sci. Alliance", "issn": "2575-1077", "volume": "5", "issue": "11", "issn-l": "2575-1077"}, "abstract": "Selective neuronal vulnerability is common in neurodegenerative diseases but poorly understood. In genetic prion diseases, including fatal familial insomnia (FFI) and Creutzfeldt-Jakob disease (CJD), different mutations in the <i>Prnp<\/i> gene manifest as clinically and neuropathologically distinct diseases. Here we report with electroencephalography studies that theta waves are mildly increased in 21 mo old knock-in mice modeling FFI and CJD and that sleep is mildy affected in FFI mice. To define affected cell types, we analyzed cell type-specific translatomes from six neuron types of 9 mo old FFI and CJD mice. Somatostatin (SST) neurons responded the strongest in both diseases, with unexpectedly high overlap in genes and pathways. Functional analyses revealed up-regulation of neurodegenerative disease pathways and ribosome and mitochondria biogenesis, and down-regulation of synaptic function and small GTPase-mediated signaling in FFI, implicating down-regulation of mTOR signaling as the root of these changes. In contrast, responses in glutamatergic cerebellar neurons were disease-specific. The high similarity in SST neurons of FFI and CJD mice suggests that a common therapy may be beneficial for multiple genetic prion diseases.", "doi": "10.26508/lsa.202201530", "pmid": "36192034", "labels": {"Bioinformatics Support, Infrastructure and Training": "Collaborative", "Bioinformatics Support and Infrastructure": "Collaborative", "Bioinformatics Support for Computational Resources": "Service", "Bioinformatics (NBIS)": "Collaborative"}, "xrefs": [{"db": "pmc", "key": "PMC9531780"}, {"db": "pii", "key": "5/11/e202201530"}], "notes": [], "created": "2022-11-09T15:50:48.068Z", "modified": "2024-01-16T13:48:34.558Z"}]}