<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Martinisi A</submitter><funding>Swiss National Science Foundation</funding><funding>the Synapsis Foundation Switzerland</funding><pagination>963-974</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8041046</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>144(3)</volume><pubmed_abstract>Tau is a microtubule stabilizing protein that forms abnormal aggregates in many neurodegenerative disorders, including Alzheimer's disease. We have previously shown that co-expression of fragmented and full-length tau in P301SxTAU62on tau transgenic mice results in the formation of oligomeric tau species and causes severe paralysis. This paralysis is fully reversible once expression of the tau fragment is halted, even though P301S tau expression is maintained. Whereas various strategies to target tau aggregation have been developed, little is known about the long-term consequences of reverted tau toxicity. Therefore, we studied the long-term motor fitness of recovered, formerly paralysed P301SxTAU62on-off mice. To assess the seeding competence of oligomeric toxic tau species, we also inocu</pubmed_abstract><journal>Brain : a journal of neurology</journal><pubmed_title>Severe oligomeric tau toxicity can be reversed without long-term sequelae.</pubmed_title><pmcid>PMC8041046</pmcid><funding_grant_id>152846</funding_grant_id><funding_grant_id>32323B_123812</funding_grant_id><funding_grant_id>310030_169486</funding_grant_id><funding_grant_id>31003A_152846</funding_grant_id><pubmed_authors>Frank S</pubmed_authors><pubmed_authors>Winkler DT</pubmed_authors><pubmed_authors>Martinisi A</pubmed_authors><pubmed_authors>Sprenger F</pubmed_authors><pubmed_authors>Flach M</pubmed_authors><pubmed_authors>Tolnay M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Severe oligomeric tau toxicity can be reversed without long-term sequelae.</name><description>Tau is a microtubule stabilizing protein that forms abnormal aggregates in many neurodegenerative disorders, including Alzheimer's disease. We have previously shown that co-expression of fragmented and full-length tau in P301SxTAU62on tau transgenic mice results in the formation of oligomeric tau species and causes severe paralysis. This paralysis is fully reversible once expression of the tau fragment is halted, even though P301S tau expression is maintained. Whereas various strategies to target tau aggregation have been developed, little is known about the long-term consequences of reverted tau toxicity. Therefore, we studied the long-term motor fitness of recovered, formerly paralysed P301SxTAU62on-off mice. To assess the seeding competence of oligomeric toxic tau species, we also inocu</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Apr</publication><modification>2025-04-04T18:37:50.139Z</modification><creation>2022-02-09T15:38:46.501Z</creation></dates><accession>S-EPMC8041046</accession><cross_references><pubmed>33484116</pubmed><doi>10.1093/brain/awaa445</doi></cross_references></HashMap>