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AofA Science Summary: Glutamate carboxypeptidase II and folate deficiencies result in reciprocal protection against cognitive and social deficits in mice

Science post imageDev Neurobiol. 2011 Nov 10. doi: 10.1002/dneu.21000. [Epub ahead of print]

Glutamate carboxypeptidase II and folate deficiencies result in reciprocal protection against cognitive and social deficits in mice: Implications for neurodevelopmental disorders.

Schaevitz LPicker JRana JKolodny NShane BBerger-Sweeney JCoyle J.


Department of Biology, Tufts University, Medford, MA 02155.


Interactions between genetic and environmental risk factors underlie a number of neuropsychiatric disorders, including schizophrenia (SZ) and autism (AD). Due to the complexity and multitude of the genetic and environmental factors attributed to these disorders, recent research strategies focus on elucidating the common molecular pathways through which these multiple risk factors may function. In this study, we examine the combined effects of a haplo-insufficiency of glutamate carboxypeptidase II (GCPII) and dietary folic acid deficiency. In addition to serving as a neuropeptidase, GCPII catalyzes the absorption of folate. GCPII and folate depletion interact within the one-carbon metabolic pathway and/or of modulate the glutamatergic system. Four groups of mice were tested: wildtype, GCPII hypomorphs, and wildtypes and GCPII hypomorphs both fed a folate deficient diet. Due to sex differences in the prevalence of SZ and AD, both male and female mice were assessed on a number of behavioral tasks including locomotor activity, rotorod, social interaction, pre-pulse inhibition, and spatial memory. Wildtype mice of both sexes fed a folic acid deficient diet showed motor coordination impairments and cognitive deficits, while social interactions were decreased only in males. GCPII mutant mice of both sexes also exhibited reduced social propensities. In contrast, all folate-depleted GCPII hypomorphs performed similarly to untreated wildtype mice, suggesting that reduced GCPII expression and folate deficiency are mutually protective. Analyses of folate and neurometabolite levels associated with glutamatergic function suggest several potential mechanisms through which GCPII and folate may be interacting to create this protective effect. © 2011 Wiley Periodicals, Inc. Develop Neurobiol, 2011.

Copyright © 2011 Wiley Periodicals, Inc.


Jenny Allan

A bit of history regarding Brian Deer's unqualified published commentary in connection with the Lancet 12 childrens' histopathology results:-
"MMR doctor Andrew Wakefield fixed data on autism" Murdoch's Sunday Times Feb 2009

"Hospital pathologists, looking for inflammatory bowel disease, reported in the majority of cases that the gut was normal. This was then reviewed and the Lancet paper showed them as abnormal."
“Wakefield’s “autistic enterocolitis” under the microscope” BMJ April 2010

“The biopsy slides are no longer available, according to one of the paper’s authors, Professor Amar Dhillon, but the GMC obtained all but one of the hospital pathology reports, and for the missing case I obtained the discharge summary. I passed the summary and reports to specialists for their reaction. They concluded that most of the 11 children reported as having non-specific colitis in the Lancet paper had been reported by the Royal Free as having normal pathology”

Sounds familiar? The ‘specialists’ Deer refers to in this article are ,” Karel Geboes, a professor in the gastrointestinal pathology unit of the Catholic University of Leuven, Belgium, and Ingvar Bjarnason, of King’s College London, a gastroenterologist with extensive paediatric experience, and a clinician with strongly expressed views AGAINST diagnosing bowel disorders in children using colonoscopies.

These are the same ‘experts’ recently quoted in the BMJ in response to David Lewis’s recent BMJ letter. As far as I can ascertain, neither of these ‘experts’ has specialist histopathology qualifications. Deer, of course, has NO medical or scientific qualifications whatsoever.
‘Pathology reports solve “new bowel disease” riddle’ Brian Deer, BMJ Nov 2011
‘Commentary: We came to an overwhelming and uniform opinion that these reports do not show colitis’ Ingvar Bjarnason, BMJ Nov 2011
Commentary: I see no convincing evidence of “enterocolitis,” “colitis,” or a “unique disease process” Karel Geboes,BMJ Nov 2011

Professor Dhillon's dignified and measured BMJ response to Brian Deer's latest BMJ broadside against the Wakefield et al 1998 Lancet study appears to confirm research procedures and recordings at the Royal Free were carried out in accordance with accepted protocols. This was 13 years ago and yes, as Mr Millar correctly points out many of Dr Wakefield's hypotheses, including ASD/bowel disorders links, have now been quietly incorporated into the established medical literature:- BMJ Rapid Response Nov 2011
Professor Dhillon states:-
“Several expert gastrointestinal pathologists and gastroenterologists have commented on the grading sheets (BMJ Nov 12 2011) and they have stated that the findings cannot be colitis; however:
-It is a mistake to apply uncritically adult gastrointestinal biopsy histopathological thresholds of normality vs abnormality to children
-The expert gastrointestinal pathologist and gastroenterologist commentators have tried to assess the diagnostic implications of data represented in histopathological grading sheets alone
-This is a fundamental mistake: the significance of the histopathological component of any diagnostic equation depends on consideration of the histopathology within the complete clinical context
- The current opinions of the experts regarding the significance of the histology grading sheets are subject to retrospective bias by knowledge of events since 1998.”


Pathogens cause disease. They get in when you have chronic inflammation. Inflammation calls for 1,25D to be made to signal your DNA to make antimicrobials. Excess 1,25D is made from 25D (I bet your doc said you were 25D deficient but you're really in chronic inflammation). Too much steroid 1,25D de-sensitizes the VDR receptor that makes over 1000 genes.
Here's just one of many studies that link pathogens to disease:
Schizophrenia: A Pathogenic Autoimmune Disease Caused by Viruses and Pathogens and Dependent on Genes

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