{"id":35125,"date":"2013-04-26T23:13:06","date_gmt":"2013-04-27T03:13:06","guid":{"rendered":"http:\/\/1boringoldman.com\/?p=35125"},"modified":"2013-04-26T23:18:14","modified_gmt":"2013-04-27T03:18:14","slug":"of-mice-and-men","status":"publish","type":"post","link":"https:\/\/1boringoldman.com\/index.php\/2013\/04\/26\/of-mice-and-men\/","title":{"rendered":"of mice and men…"},"content":{"rendered":"

So what pollen does to the brain is make things fuzzy and they get lost in the sulcus-scape. This is a thread I lost three weeks ago that I wanted to follow up on – an article by Dr. Steven Hyman, former Director of the NIMH [see Psychiatric Drug Development: Diagnosing a Crisis<\/a>, whither the crisis…<\/a>, notwithstanding…<\/a>, the biggest point…<\/a>, Walk the Walk<\/a>]. Like so many of his colleagues, he was talking about the crisis<\/em> in the development of psychiatric drugs. In the article, he seems to be blaming the "forced swim test," an animal model used to evaluate drugs for antidepressant properties, for some of the lack of progress. A reminder: <\/p>\n

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Psychiatric Drug Development: Diagnosing a Crisis<\/a>
The Dana Foundation: Cerebrum<\/font><\/strong>
By Steven E. Hyman
April 02, 2013<\/div>\n

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The antidepressant drug imipramine prolongs the period during which the rat attempts to swim. This forced swim assay was rationalized with anthropomorphic terms such as “behavioral despair,” but it was never shown to model human depression…<\/strong><\/sup> Despite some degree of surface plausibility — the forced swim result seemed to mimic learned helplessness, a putative model of depression — the mechanism by which imipramine causes continued swimming is still not known. Moreover, imipramine increases the duration of swimming with a single dose, whereas depressed human beings generally require several weeks of treatment before therapeutic effects emerge… From the very beginning, however, astute scientists predicted that this approach to drug development would result in the identification of only “me too” drugs. Unfortunately, during the last 50 years that concern has been fully borne out…<\/strong><\/sup> <\/div>\n<\/blockquote>\n

This was not a new point for Dr. Hyman. He’d made it in a review article with Eric Nester in 2010 and had mentioned it in a variety of recent presentations: <\/p>\n

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Animal models of neuropsychiatric disorders.
by Nestler EJ and Hyman SE.<\/strong><\/sup>
Nature Neuroscience<\/font><\/strong>. 2010 13(10):1161-9.<\/div>\n

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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.<\/strong><\/sup><\/div>\n<\/blockquote>\n
And from the text of the review: <\/div>\n