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Raux G, Bumsel E, Hecketsweiler B, van Amelsvoort T, Zinkstok J, Manouvrier-Hanu S, Fantini C, Brévière GM, Di Rosa G, Pustorino G, Vogels A, Swillen A, Legallic S, Bou J, Opolczynski G, Drouin-Garraud V, Lemarchand M, Philip N, Gérard-Desplanches A, Carlier M, Philippe A, Nolen MC, Heron D, Sarda P, Lacombe D, Coizet C, Alembik Y, Layet V, Afenjar A, Hannequin D, Demily C, Petit M, Thibaut F, Frebourg T, Campion D. Involvement of hyperprolinemia in cognitive and psychiatric features of the 22q11 deletion syndrome. Hum Mol Genet . 2007 Jan 1 ; 16(1):83-91. PubMed Abstract

Comments on Paper and Primary News
Comment by:  Carrie Bearden
Submitted 17 December 2006 Posted 17 December 2006

It is now well known that patients with 22q11.2 deletions have substantially elevated rates of psychotic illness. Multiple investigations have attempted to elucidate the specific mechanisms underlying the development of psychosis in some patients with this syndrome but not others. Given its role in prefrontal cortical dopamine metabolism, the COMT gene (located within the 22q11.2 deleted region) is of course a compelling candidate gene for this phenotype, although the evidence for this is equivocal (e.g. Murphy et al., 1999). In addition, mechanisms underlying variability in other CNS features of the VCFS phenotype have yet to be determined. For example, there is considerable variability in the cognitive phenotype, with IQ’s ranging from severe mental retardation to the average range, but the specific genes (and other epigenetic factors) that may be relevant to cognitive function in this syndrome are not clear.

Here, Raux and colleagues show that a subset of VCFS patients with severe...  Read more

View all comments by Carrie Bearden

Comment by:  Mary Reid
Submitted 17 December 2006 Posted 18 December 2006

In response to Carrie Bearden, I wonder whether these patients who suffer cognitive deficits and neuropsychiatric disease associated with 22q11.2 deletion syndrome may benefit specifically from alpha-Tocopherol and ascorbic acid? Delwing and colleagues find that these vitamins prevent memory deficits in rats with hyperprolinemia. Also of interest is the study by Kern and Bernards finding that ascorbic acid inhibits spinal meningeal COMT activity.


Delwing D, Bavaresco CS, Monteiro SC, Matte C, Netto CA, Wyse AT. alpha-Tocopherol and ascorbic acid prevent memory deficits provoked by chronic hyperprolinemia in rats. Behav Brain Res. 2006 Apr 3;168(2):185-9. Epub 2005 Oct 6. Abstract

Kern C, Bernards CM. Ascorbic acid inhibits spinal meningeal catechol-o-methyl transferase in vitro, markedly increasing epinephrine bioavailability. Anesthesiology. 1997 Feb;86(2):405-9. Abstract

View all comments by Mary Reid

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