Animal Models of Neuropsychiatric Disorders
By E. Nestler, S. Hyman. Nature Neuroscience, 2010
2,057 citations recorded by the source corpus.
Modeling of human neuropsychiatric disorders in animals is extremely challenging given the subjective nature of many symptoms, the lack of biomarkers and objective diagnostic tests, and the early state of the relevant neurobiology and genetics. Nonetheless, progress in understanding pathophysiology and in treatment development would benefit greatly from improved animal models. Here we review the current state of animal models of mental illness, with a focus on schizophrenia, depression and bipolar disorder. We argue for areas of focus that might increase the likelihood of creating more useful models, at least for some disorders, and for explicit guidelines when animal models are reported.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Social Psychology
View Paper: https://www.semanticscholar.org/paper/412a54e8eefbccf69be2c2882f2912961e18808f
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In Cellular and Molecular Neuroscience
- P. Belujon
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- Scott J. Webster
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In Molecular Biology
In Social Psychology
Citations in the corpus
- Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models (2014, background): “…applicable tools to study depression in animal models (Seligman et al., 1975; Jolly et al., 1999; Song and Leonard, 2005; Flint and Shifman, 2008; Nestler and Hyman, 2010), very little work has been devoted to determining the range of depressive behavioral symptoms in the commonly used mouse…”
- Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities and core autism-related deficits (2011, neutral): “Ideally, mouse models should be based on a known genetic cause of the disease (construct validity), reflect key aspects of the human symptoms (face validity), and respond to treatments that are effective in the human disease (predictive validity) (Chadman et al., 2009; Nestler and Hyman, 2010).”
- Rethinking schizophrenia (2010, background): “well as the identification of subtle clinical features, we are beginning to detect earlier stages of risk and prodrome.(67)”
- Scaling Brain Size, Keeping Timing: Evolutionary Preservation of Brain Rhythms (2013, neutral): “Unlike the widely varying drug responses between humans and animal models across many measures (Nestler and Hyman, 2010), the pharmacological profiles of network oscillations are most likely identical in all mammalian species.”
- Dopamine System Dysregulation in Major Depressive Disorders (2017, background): “Indeed, animals exposed to this procedure show weight loss, alterations in sleep patterns, modification of the hypothalamopituitary-adrenal axis activity, and a decrease in spine density in the hippocampus and the mPFC (Nestler and Hyman, 2010; Yang et al., 2015).”