Microtubule and microtubule associated protein anomalies in psychiatric disease
Anomalies in neuronal cell architecture, in particular dendritic complexity and synaptic density changes, are widely observed in the brains of subjects with schizophrenia or mood disorders. The concept that a disturbed microtubule cytoskeleton underlies these abnormalities and disrupts synaptic conn...
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| Published in | Cytoskeleton (Hoboken, N.J.) Vol. 73; no. 10; pp. 596 - 611 |
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| Main Authors | , , |
| Format | Journal Article |
| Language | English |
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United States
Blackwell Publishing Ltd
01.10.2016
Wiley Subscription Services, Inc |
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| Abstract | Anomalies in neuronal cell architecture, in particular dendritic complexity and synaptic density changes, are widely observed in the brains of subjects with schizophrenia or mood disorders. The concept that a disturbed microtubule cytoskeleton underlies these abnormalities and disrupts synaptic connectivity is supported by evidence from clinical studies and animal models. Prominent changes in tubulin expression levels are commonly found in disease specific regions such as the hippocampus and prefrontal cortex of psychiatric patients. Genetic linkage studies associate tubulin‐binding proteins such as the dihydropyrimidinase family with an increased risk to develop schizophrenia and bipolar disorder. For many years, altered immunoreactivity of microtubule associated protein‐2 has been a hallmark found in the brains of individuals with schizophrenia. In this review, we present a growing body of evidence that connects a dysfunctional microtubule cytoskeleton with neuropsychiatric illnesses. Findings from animal models are discussed together with clinical data with a particular focus on tubulin post‐translational modifications and on microtubule‐binding proteins. © 2016 Wiley Periodicals, Inc. |
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| AbstractList | Anomalies in neuronal cell architecture, in particular dendritic complexity and synaptic density changes, are widely observed in the brains of subjects with schizophrenia or mood disorders. The concept that a disturbed microtubule cytoskeleton underlies these abnormalities and disrupts synaptic connectivity is supported by evidence from clinical studies and animal models. Prominent changes in tubulin expression levels are commonly found in disease specific regions such as the hippocampus and prefrontal cortex of psychiatric patients. Genetic linkage studies associate tubulin‐binding proteins such as the dihydropyrimidinase family with an increased risk to develop schizophrenia and bipolar disorder. For many years, altered immunoreactivity of microtubule associated protein‐2 has been a hallmark found in the brains of individuals with schizophrenia. In this review, we present a growing body of evidence that connects a dysfunctional microtubule cytoskeleton with neuropsychiatric illnesses. Findings from animal models are discussed together with clinical data with a particular focus on tubulin post‐translational modifications and on microtubule‐binding proteins. © 2016 Wiley Periodicals, Inc. |
| Author | Coffey, Eleanor T. Marchisella, Francesca Hollos, Patrik |
| Author_xml | – sequence: 1 givenname: Francesca surname: Marchisella fullname: Marchisella, Francesca organization: Turku Centre for Biotechnology, Åbo Akademi University and University of Turku, Finland – sequence: 2 givenname: Eleanor T. surname: Coffey fullname: Coffey, Eleanor T. email: ecoffey@btk.fi, ecoffey@btk.fi organization: Turku Centre for Biotechnology, Åbo Akademi University and University of Turku, Finland – sequence: 3 givenname: Patrik surname: Hollos fullname: Hollos, Patrik organization: Turku Centre for Biotechnology, Åbo Akademi University and University of Turku, Finland |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27112918$$D View this record in MEDLINE/PubMed |
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| Title | Microtubule and microtubule associated protein anomalies in psychiatric disease |
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