Mouse Models of Schizophrenia and Bipolar Disorder

Author(s):  
Mikhail V. Pletnikov ◽  
Christopher A. Ross

Despite the recent advances in research into schizophrenia and bipolar disorder, the neurobiology of these maladies remains poorly understood. Animal models can be instrumental in elucidating the underlying mechanisms of neuropsychiatric disorders. Early animal models of schizophrenia and bipolar disorder used lesion methods, pharmacologic challenges or environmental interventions to mimic pathogenic features of the diseases. The recent progress in genetics has stimulated the development of etiological models that have begun to provide insight into pathogenesis. In this review, we evaluate the strengths and weaknesses of the existing genetic mouse models of schizophrenia and discuss potential developments for the future.

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Timir Datta-Chaudhuri

AbstractMouse models have been of tremendous benefit to medical science for the better part of a century, yet bioelectronic medicine research using mice has been limited to mostly acute studies because of a lack of tools for chronic stimulation and sensing. A wireless neuromodulation platform small enough for implantation in mice will significantly increase the utility of mouse models in bioelectronic medicine. This perspective examines the necessary functionality of such a system and the technical challenges needed to be overcome for its development. Recent progress is examined and the outlook for the future of implantable devices for mice is discussed.


Author(s):  
Craig M. Powell ◽  
Antony A. Boucard

Animal models of autism are now prolific as human genetic findings in autism provide a compelling rationale for developing bona fide mouse models of subtypes of human autism/mental retardation. Furthermore, these findings provide the opportunity to understand at a molecular, cellular, and circuit level the pathogenesis of a subset of ASDs. This chapter introduces neuroligins and neurexins, their function, their genetic link to autism, genetic mouse models of autism based on neuroligin and neurexin mutation/deletion, and the potential for understanding the pathogenesis and ultimately treatment of ASDs linked to these genes. This chapter is updated and adapted from an earlier published version (Powell & Boucard, 2010).


2015 ◽  
Vol 141 ◽  
pp. 42-56 ◽  
Author(s):  
Kimberly A. Fernandes ◽  
Jeffrey M. Harder ◽  
Pete A. Williams ◽  
Rebecca L. Rausch ◽  
Amy E. Kiernan ◽  
...  

2019 ◽  
Vol 2 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Pike-See Cheah ◽  
John O. Mason ◽  
King Hwa Ling

The human brain is made up of billions of neurons and glial cells which are interconnected and organized into specific patterns of neural circuitry, and hence is arguably the most sophisticated organ in human, both structurally and functionally. Studying the underlying mechanisms responsible for neurological or neurodegenerative disorders and the developmental basis of complex brain diseases such as autism, schizophrenia, bipolar disorder, Alzheimer’s and Parkinson’s disease has proven challenging due to practical and ethical limitations on experiments with human material and the limitations of existing biological/animal models. Recently, cerebral organoids have been proposed as a promising and revolutionary model for understanding complex brain disorders and preclinical drug screening.


Endocrinology ◽  
2008 ◽  
Vol 149 (12) ◽  
pp. 5952-5957 ◽  
Author(s):  
I. Torres-Aleman

It is lay knowledge now that Alzheimer’s dementia (AD) is one of the most devastating diseases afflicting our societies. A major thrust in search for a cure has relied in the development of animal models of the disease. Thanks to progress in the genetics of the rare inherited forms of AD, various transgenic mouse models harboring human mutated proteins were developed, yielding very significant advancements in the understanding of pathological pathways. Although these models led to testing many different new therapies, none of the preclinical successes have translated yet into much needed therapeutic improvements. Further insight into the metabolic disturbances that are probably associated with the onset of the disease may also rely on new animal models of AD involving insulin/IGF-I signaling that could mimic the far most common sporadic forms of AD associated with old age. Combination of models of familial AD that develop severe amyloidosis with those displaying defects in insulin/IGF-I signaling may help clarify the link between putative initial metabolic disturbances and mechanisms of pathological progression.


2019 ◽  
Vol 19 (3) ◽  
pp. 229-234 ◽  
Author(s):  
Hua Yang ◽  
Hong-Min Ni ◽  
Wen-Xing Ding

Studies using genetic mouse models that have defective autophagy have led to the conclusion that macroautophagy/autophagy serves as a tumor suppressor. One of such models is the liver-specific Atg5 or Atg7 knockout mice, and these knockout mice develop spontaneous liver tumors. It has been generally agreed that p62-mediated Nrf2 activation plays a critical role in promoting autophagy deficiency-induced liver injury and liver tumorigenesis. The mechanisms of how persistent Nrf2 activation induces liver injury and tumorigenesis are incompletely known. We discuss the recent progress on the new roles of HMGB1 and Yap in regulating liver injury and tumorigenesis in mice with liver-specific autophagy deficiency.


2016 ◽  
Vol 2016 ◽  
pp. 1-23 ◽  
Author(s):  
Paula Moran ◽  
Jennifer Stokes ◽  
Julia Marr ◽  
Gavin Bock ◽  
Lieve Desbonnet ◽  
...  

The study of gene × environment, as well as epistatic interactions in schizophrenia, has provided important insight into the complex etiopathologic basis of schizophrenia. It has also increased our understanding of the role of susceptibility genes in the disorder and is an important consideration as we seek to translate genetic advances into novel antipsychotic treatment targets. This review summarises data arising from research involving the modelling of gene × environment interactions in schizophrenia using preclinical genetic models. Evidence for synergistic effects on the expression of schizophrenia-relevant endophenotypes will be discussed. It is proposed that valid and multifactorial preclinical models are important tools for identifying critical areas, as well as underlying mechanisms, of convergence of genetic and environmental risk factors, and their interaction in schizophrenia.


2013 ◽  
Vol 3 (11) ◽  
pp. 1881-1891 ◽  
Author(s):  
Muhammad Farooq Rai ◽  
Eric J. Schmidt ◽  
Audrey McAlinden ◽  
James M. Cheverud ◽  
Linda J. Sandell

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