FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2016496193> ?p ?o ?g. }

• W2016496193 abstract "Recently, we and others reported that aged-tau knockout mice exhibit behavioural deficits, arguing for a role of functional tau protein in brain health. We also showed that these mice exhibit iron-dependent neurodegeneration and clioquinol (CQ), a drug that binds to iron, prevented the development of symptoms in tau KO mice. However, prospective treatments for neurodegenerative disorders will need to confer benefit to symptomatic patients. Here, CQ was given to symptomatic 12-months old tau KO mice to test whether this treatment was effective. Tau knockout mice (tau KO) and background C57BL6/SV129 control mice (WT), at 12 months of age, were treated with CQ chow (30mg/kg body weight /day) for 5.5 months. We monitored the mice by pole test and rotarod every three weeks during treatment period, and terminated this study when the mice were 17-months of age. Y maze tests were performed before the mice being euthanized for biochemical studies. Tyrosine hydroxylase staining was used for stereological estimation of nigral neurons. Dopamine was measured by HPLC. Before treatment commenced, tau KO mice exhibited cognitive loss (y-maze) and parkinsonism (rotarod, pole test), as previously reported. Over the course of the study, CQ treatment reversed the motor and cognitive impairment as evidenced by improvement in the Pole test (P<0.001) and Rotarod test (P=0.008) and y-maze (P=0.038). Restoration of behavioral disability reflected preservation of neuroanatomical features including enlargement of cortical thickness (P=0.026) and striatal enlargement (P=0.001) and reduction of the lateral ventricular area (P<0.001) at the conclusion of the study. These benefits conferred by CQ treatment could be attributed to reduction in iron load in the brain since treatment with CQ for 5.5 months had decreased iron in the brain (P=0.003 for hippocampus, and P=0.007 for SN) but not liver. Copper and zinc levels were unaffected. Here we report that iron chelation by CQ rescued several neurodegenerative phenotypes of aged tau KO mice, further supporting our hypothesis that tau plays a crucial role in age-related diseases. Importantly, these benefits were conferred to mice that began treatment after symptom manifestation, highlighting the potential for iron chelation approaches as disease modifying therapeutics for neurodegenerative diseases." @default.
• W2016496193 created "2016-06-24" @default.
• W2016496193 creator A5018022715 @default.
• W2016496193 creator A5043595615 @default.
• W2016496193 creator A5048261317 @default.
• W2016496193 creator A5067513465 @default.
• W2016496193 date "2013-07-01" @default.
• W2016496193 modified "2023-09-27" @default.
• W2016496193 title "DT-03-05: Rescue of Behavioral and neurodegenerative phenotypes in symptomatic tau KO mice: Therapeutic implications for neurodegenerative diseases" @default.
• W2016496193 doi "https://doi.org/10.1016/j.jalz.2013.08.017" @default.
• W2016496193 hasPublicationYear "2013" @default.
• W2016496193 type Work @default.
• W2016496193 sameAs 2016496193 @default.
• W2016496193 citedByCount "0" @default.
• W2016496193 crossrefType "journal-article" @default.
• W2016496193 hasAuthorship W2016496193A5018022715 @default.
• W2016496193 hasAuthorship W2016496193A5043595615 @default.
• W2016496193 hasAuthorship W2016496193A5048261317 @default.
• W2016496193 hasAuthorship W2016496193A5067513465 @default.
• W2016496193 hasBestOaLocation W20164961931 @default.
• W2016496193 hasConcept C126322002 @default.
• W2016496193 hasConcept C134018914 @default.
• W2016496193 hasConcept C15744967 @default.
• W2016496193 hasConcept C159167319 @default.
• W2016496193 hasConcept C169760540 @default.
• W2016496193 hasConcept C2776525014 @default.
• W2016496193 hasConcept C2776925932 @default.
• W2016496193 hasConcept C2777981454 @default.
• W2016496193 hasConcept C2779134260 @default.
• W2016496193 hasConcept C2781161787 @default.
• W2016496193 hasConcept C2985495968 @default.
• W2016496193 hasConcept C44752575 @default.
• W2016496193 hasConcept C513476851 @default.
• W2016496193 hasConcept C71924100 @default.
• W2016496193 hasConceptScore W2016496193C126322002 @default.
• W2016496193 hasConceptScore W2016496193C134018914 @default.
• W2016496193 hasConceptScore W2016496193C15744967 @default.
• W2016496193 hasConceptScore W2016496193C159167319 @default.
• W2016496193 hasConceptScore W2016496193C169760540 @default.
• W2016496193 hasConceptScore W2016496193C2776525014 @default.
• W2016496193 hasConceptScore W2016496193C2776925932 @default.
• W2016496193 hasConceptScore W2016496193C2777981454 @default.
• W2016496193 hasConceptScore W2016496193C2779134260 @default.
• W2016496193 hasConceptScore W2016496193C2781161787 @default.
• W2016496193 hasConceptScore W2016496193C2985495968 @default.
• W2016496193 hasConceptScore W2016496193C44752575 @default.
• W2016496193 hasConceptScore W2016496193C513476851 @default.
• W2016496193 hasConceptScore W2016496193C71924100 @default.
• W2016496193 hasIssue "4S_Part_21" @default.
• W2016496193 hasLocation W20164961931 @default.
• W2016496193 hasOpenAccess W2016496193 @default.
• W2016496193 hasPrimaryLocation W20164961931 @default.
• W2016496193 hasRelatedWork W1979059193 @default.
• W2016496193 hasRelatedWork W2015327999 @default.
• W2016496193 hasRelatedWork W2018532868 @default.
• W2016496193 hasRelatedWork W2034255477 @default.
• W2016496193 hasRelatedWork W2060828139 @default.
• W2016496193 hasRelatedWork W2062579683 @default.
• W2016496193 hasRelatedWork W2089103608 @default.
• W2016496193 hasRelatedWork W2163744984 @default.
• W2016496193 hasRelatedWork W2171851218 @default.
• W2016496193 hasRelatedWork W2748952813 @default.
• W2016496193 hasVolume "9" @default.
• W2016496193 isParatext "false" @default.
• W2016496193 isRetracted "false" @default.
• W2016496193 magId "2016496193" @default.
• W2016496193 workType "article" @default.