Methylglyoxal, advanced glycation end products and autism: is there a connection?

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Methylglyoxal, advanced glycation end products and autism: is there a

connection? <http://www.ncbi.nlm.nih.gov/pubmed/22325990>

Maher P.

Med Hypotheses. 2012 Apr;78(4):548-52.

Autism is a complex and heterogeneous neurodevelopmental disorder of

unknown etiology but very likely resulting from both genetic and

environmental factors. Recent estimates suggest that it affects 1 in

100-150 individuals in the US. Oxidative stress, inflammation and

mitochondrial dysfunction have all been suggested to play key roles in

autism and may be linked via alterations in cellular redox homeostasis.

The glutathione/glutathione disulfide (GSH/GSSG) redox pair forms the

major redox couple in cells and as such plays a critical role in

regulating redox-dependent cellular functions. A number of studies have

shown that variations in genes involved in GSH metabolism are associated

with autism. GSH also modulates the activity of glyoxalase 1 (Glo-1),

the rate-limiting enzyme for the removal of reactive dicarbonyls such as

methylglyoxal (MG). MG is the major precursor for the formation of

advanced glycation end products (AGEs). Both MG and AGEs can induce

oxidative stress, inflammation and mitochondrial dysfunction and are

implicated in diabetic complications and multiple, age-related

neurological diseases. Dietary consumption of AGEs and MG correlates

with food intake which has increased 20-30% over the past 20 years. Both

MG and AGEs are orally absorbed, leading to increased levels in the

blood. Furthermore, in humans, increased MG and AGE levels in maternal

blood correlate with increased MG and AGE levels in newborn blood,

potentially exposing infants to high oxidative stress and inflammation.

It is hypothesized that diet derived MG and AGEs in combination with

inborn genetic vulnerabilities that affect the cellular redox status are

major contributors to the development of autism and provide a causal

link between oxidative stress, inflammation and mitochondrial

dysfunction. If future research supports this hypothesis, then by

reducing the exposure to these diet-derived factors, it might be

possible to decrease the prevalence of at least a subset of autism cases.

http://en.wikipedia.org/wiki/Methylglyoxal

http://en.wikipedia.org/wiki/Advanced_glycation_end-product

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