Researchers Have Developed a Potential Blood Test for Autism 2/18/18 Futurism.com

[*GG*]

Wonder how this might relate to work being done by Ron Davis? @Ben H and @Janet Dafoe (Rose49)

I haven't kept up with the research

"Since proteins in blood plasma can be damaged by two processes, oxidation and glycation, and the researchers developed tests that can detect that damage."

https://futurism.com/autism-blood-urine-test/

 

[andyguitar]

I had a look at this research as I think that Autism and ME have somethings in common. From my fairly limited knowledge about science my conclusion is that the relevant finding in the research is that the transporter for the amino acid Arginine does not function properly. So I would suggest that anyone who has an interest in this subject put 'Arginine' into a search engine.

 

[pattismith]

Advanced glycation endproducts, dityrosine and arginine transporter dysfunction in autism - a source of biomarkers for clinical diagnosis

• Attia Anwar†,etc

2018

Abstract
Background
Clinical chemistry tests for autism spectrum disorder (ASD) are currently unavailable. The aim of this study was to explore the diagnostic utility of proteotoxic biomarkers in plasma and urine, plasma protein glycation, oxidation, and nitration adducts, and related glycated, oxidized, and nitrated amino acids (free adducts), for the clinical diagnosis of ASD.

Methods
Thirty-eight children with ASD (29 male, 9 female; age 7.6 ± 2.0 years) and 31 age-matched healthy controls (23 males, 8 females; 8.6 ± 2.0 years) were recruited for this study. Plasma protein glycation, oxidation, and nitration adducts and amino acid metabolome in plasma and urine were determined by stable isotopic dilution analysis liquid chromatography-tandem mass spectrometry. Machine learning methods were then employed to explore and optimize combinations of analyte data for ASD diagnosis.

Results
We found that children with ASD had increased advanced glycation endproducts (AGEs),
Nε-carboxymethyl-lysine (CML)
and Nω-carboxymethylarginine (CMA),
and increased oxidation damage marker, dityrosine (DT), in plasma protein, with respect to healthy controls.

We also found that children with ASD had increased CMA free adduct in plasma ultrafiltrate
and increased urinary excretion of oxidation free adducts, alpha-aminoadipic semialdehyde and glutamic semialdehyde.

From study of renal handling of amino acids, we found that children with ASD had decreased renal clearance of arginine and CMA with respect to healthy controls.

Algorithms to discriminate between ASD and healthy controls gave strong diagnostic performance with features: plasma protein AGEs—CML, CMA—and 3-deoxyglucosone-derived hydroimidazolone, and oxidative damage marker, DT.

The sensitivity, specificity, and receiver operating characteristic area-under-the-curve were 92%, 84%, and 0.94, respectively.

Conclusions
Changes in plasma AGEs were likely indicative of dysfunctional metabolism of dicarbonyl metabolite precursors of AGEs, glyoxal and 3-deoxyglucosone. DT is formed enzymatically by dual oxidase (DUOX); selective increase of DT as an oxidative damage marker implicates increased DUOX activity in ASD possibly linked to impaired gut mucosal immunity. Decreased renal clearance of arginine and CMA in ASD is indicative of increased arginine transporter activity which may be a surrogate marker of disturbance of neuronal availability of amino acids. Data driven combination of these biomarkers perturbed by proteotoxic stress, plasma protein AGEs and DT, gave diagnostic algorithms of high sensitivity and specificity for ASD.