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Annotation

Meyer-Lindenberg A, Straub RE, Lipska BK, Verchinski BA, Goldberg T, Callicott JH, Egan MF, Huffaker SS, Mattay VS, Kolachana B, Kleinman JE, Weinberger DR. Genetic evidence implicating DARPP-32 in human frontostriatal structure, function, and cognition. J Clin Invest . 2007 Mar ; 117(3):672-82. PubMed Abstract

Comments on Paper and Primary News
Primary News: DARPP-32 Haplotype Affects Frontostriatal Cognition and Schizophrenia Risk

Comment by:  Jonathan Burns
Submitted 14 February 2007 Posted 14 February 2007

This study provides hard empirical evidence for the hypothesis that psychosis (and schizophrenia in particular) represents a costly "byproduct" of complex human (social) brain evolution. Interestingly, the activation paradigms in the fMRI study (N-back and emotional face-matching tasks) are both testing social cognition. And the demonstrated changes in frontostriatal connectivity support the hypothesis that schizophrenia is a disorder of evolved intrahemispheric circuits comprising the Social Brain in our species.

I would suggest that further candidates (conferring vulnerability to psychosis) should be sought from amongst those genes known to have played a significant role in human brain evolution.

References:

Burns J. (2007) The Descent of Madness: Evolutionary Origins of Psychosis and the Social Brain. Routledge Press: Hove, Sussex.

Burns J. The social brain hypothesis of schizophrenia. World Psychiatry. 2006 Jun;5(2):77-81. Abstract

Burns JK. Psychosis: a costly by-product of social brain evolution in Homo sapiens. Prog Neuropsychopharmacol Biol Psychiatry. 2006 Jul;30(5):797-814. Epub 2006 Mar 3. Review. Abstract

Burns JK. An evolutionary theory of schizophrenia: cortical connectivity, metarepresentation, and the social brain. Behav Brain Sci. 2004 Dec;27(6):831-55; discussion 855-85. Review. Abstract

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Primary News: DARPP-32 Haplotype Affects Frontostriatal Cognition and Schizophrenia Risk

Comment by:  Daniel Durstewitz
Submitted 8 June 2007 Posted 8 June 2007
  I recommend this paper

The phosphoprotein DARPP-32 occupies a central position in the dopamine-regulated intracellular cascades of cortical and striatal neurons (Greengard et al., 1999). It is a point of convergence for multiple signaling pathways, is differentially affected by D1- vs. D2-class receptor activation, and mainly through inhibition of protein-phosphotase-1 mediates or contributes to a number of the dopaminergic effects on voltage- and ligand-gated ion channels. These, in turn, by regulating intracellular Ca2+ levels, themselves influence phosphorylation of DARPP-32 and thereby interact with dopamine-induced processes.

Given its central, vital role in dopamine-regulated signaling pathways, it is quite surprising that (to my knowledge) only a few studies exist on the implications of DARPP-32 variations for cognitive functions and brain activity. Therefore, this comprehensive series of studies by Meyer-Lindenberg et al. combining human genetics, structural and functional MRI, and behavioral testing represents an important milestone....  Read more


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