<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Krupp S</submitter><funding>NIA NIH HHS</funding><pubmed_abstract>Accumulation of cytoplasmic inclusions of TAR-DNA binding protein 43 (TDP-43) is seen in both neurons and glia in a range of neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Alzheimer's disease (AD). Disease progression involves non-cell autonomous interactions among multiple cell types, including neurons, microglia and astrocytes. We investigated the effects in &lt;i>Drosophila&lt;/i> of inducible, glial cell type-specific TDP-43 overexpression, a model that causes TDP-43 protein pathology including loss of nuclear TDP-43 and accumulation of cytoplasmic inclusions. We report that TDP-43 pathology in &lt;i>Drosophila&lt;/i> is sufficient to cause progressive loss of each of the 5 glial sub-types. But the effects on organismal survival were m</pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2023.05.04.539439</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10187300</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>TDP-43 pathology in &lt;i>Drosophila&lt;/i> induces glial-cell type specific toxicity that can be ameliorated by knock-down of SF2/SRSF1.</pubmed_title><pmcid>PMC10187300</pmcid><funding_grant_id>RF1 AG076493</funding_grant_id><funding_grant_id>R01 AG078788</funding_grant_id><funding_grant_id>RF1 AG057338</funding_grant_id><pubmed_authors>Krupp S</pubmed_authors><pubmed_authors>Tam O</pubmed_authors><pubmed_authors>Hammell MG</pubmed_authors><pubmed_authors>Dubnau J</pubmed_authors></additional><is_claimable>false</is_claimable><name>TDP-43 pathology in &lt;i>Drosophila&lt;/i> induces glial-cell type specific toxicity that can be ameliorated by knock-down of SF2/SRSF1.</name><description>Accumulation of cytoplasmic inclusions of TAR-DNA binding protein 43 (TDP-43) is seen in both neurons and glia in a range of neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Alzheimer's disease (AD). Disease progression involves non-cell autonomous interactions among multiple cell types, including neurons, microglia and astrocytes. We investigated the effects in &lt;i>Drosophila&lt;/i> of inducible, glial cell type-specific TDP-43 overexpression, a model that causes TDP-43 protein pathology including loss of nuclear TDP-43 and accumulation of cytoplasmic inclusions. We report that TDP-43 pathology in &lt;i>Drosophila&lt;/i> is sufficient to cause progressive loss of each of the 5 glial sub-types. But the effects on organismal survival were m</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 May</publication><modification>2025-06-25T03:04:20.439Z</modification><creation>2025-06-25T03:04:20.439Z</creation></dates><accession>S-EPMC10187300</accession><cross_references><pubmed>37205372</pubmed><doi>10.1101/2023.05.04.539439</doi></cross_references></HashMap>