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> Here are slides prepared by Jeff Bradstreet about Thimerosal &

MTHFR

> and Jill ' paper about MTHFR

> Jane

Here is one interesting aspect that doesn't appear to validate some

of the connections I see being made. There was mention of exposure

leading to problems with IGF-1, dopamine and caspase-3. Research on

CFS has shown that caspase-3 is not elevated and the research below

could also be interpreted the same for autism. At least the fatty

acids shown are exactly opposite.

Geier uses Baskins research as a reference to help back his theory.

Baskin DS et al. Toxicol Sci. 2003 Aug;74(2):361-8.

" Mercury-induced intracellular calcium modulated reactive oxygen

species (ROS) production, which resulted in both cell apoptosis and

necrosis indicated by annexin V binding and caspase-3 activity "

Baskin DS, Ngo H, Didenko VV.

Thimerosal induces DNA breaks, caspase-3 activation, membrane

damage, and cell death in cultured human neurons and fibroblasts.

Toxicol Sci. 2003 Aug;74(2):361-8. Epub 2003 May 28.

PMID: 12773768 [PubMed - indexed for MEDLINE]

Comp Biochem Physiol B Biochem Mol Biol. 2003 Nov;136(3):521-32.

Homocysteine-induced changes in brain membrane composition correlate

with increased brain caspase-3 activities and reduced chick embryo

viability.

RR, Leanza CM, EE, Blacquire KD.

Hillsdale College, Biology Department, 33 E College, Hillsdale, MI

49242-1205, USA. bob.miller@...

In adult systems, high homocysteine (HoCys) levels inhibit

methylation reactions and can induce apoptosis in the central

nervous system. In embryos, exogenous HoCys is teratogenic and is

associated with neural tube defects. Because, methylation inhibitors

and inducers of apoptosis can influence membrane composition, we

have studied whether or not embryonic exposure to HoCys influenced

membrane phospholipid levels, membrane fatty acid composition, and

Caspase-3 activities in embryonic chick brains. Embryonic exposure

to HoCys caused reduced brain phosphatidylcholine levels and

**increased*** levels of brain phosphatidylethanolamine. Exogenous

HoCys also promoted decreased levels of long-chain, unsaturated

membrane fatty acids and increased levels of saturated short-chain

membrane fatty acids.

These HoCys-induced brain membrane changes correlated with HoCys-

induced increases in brain Caspase-3 activities, HoCys-induced

reductions in brain mass, HoCys-induced reductions in embryo mass,

and HoCys-induced reductions in the percentage of embryos that

survived to 11 days of development (theoretical stage 37). Thus,

HoCys-induced changes in brain membrane composition correlated with

HoCys-induced apoptosis and reduced embryo viability.

PMID: 14602160 [PubMed - in process]

Life Sci. 2004 Feb 13;74(13):1635-43.

Alteration in amino-glycerophospholipids levels in the plasma of

children with autism: a potential biochemical diagnostic marker.

Chauhan V, Chauhan A, Cohen IL, Brown WT, Sheikh A.

NYS Institute for Basic Research in Developmental Disabilities,

Staten Island, New York, NY 10314, USA. chauhanvps@...

Currently, there is no biochemical test to assist in the behavioral

diagnosis of autism. We observed that levels of

phosphatidylethanolamine (PE) were **decreased** while

phosphatidylserine (PS) were increased in the erythrocyte membranes

of children with autism as compared to their non-autistic

developmentally normal siblings. A

new method using Trinitrobenezene sulfonic acid (TNBS) for the

quantification of PE and PS (amino-glycerophospholipids, i.e., AGP)

in the plasma of children was developed and standardized. Wavelength

scans of TNBS-PE and TNBS-PS complexes gave two peaks at 320 nm and

410 nm. When varying concentrations of PS and PE were used, a linear

regression line was observed at 410 nm with TNBS. Using this assay,

the levels of AGP were found to be significantly increased in the

plasma of children with autism as compared to their non-autistic

normal siblings. It is proposed that plasma AGP levels may function

as a potential diagnostic marker for autism.

PMID: 14738907 [PubMed - indexed for MEDLINE]

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  • 3 years later...

Hi

I have just come from a visit with the allergist with my 5 yr old who

has CMT1A.

He has a blood mutation is how he put it called MTHFR which stops the

ability to process B12 Folic acid Vitamin C.

Does anyone know if this could be associated to the CMT or just another

gift?

Any help or knowledge would be wonderful.

Thanks heaps

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