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A proposed link between aging, autism, and oxidation

Print this Page   Home > News > 2013 > A proposed link between aging, autism, and oxidation

March 01, 2013

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Like any fac­tory, the body burns oxygen to get energy for its var­ious needs. As a result, detri­mental byprod­ucts are released and our cells try to clean up shop with antiox­i­dants. But as we age, this process becomes a losing battle.

"Oxi­da­tion inex­orably moves us along toward an oxi­dized state," said phar­ma­ceu­tical sci­ences pro­fessor Richard Deth. "You have to deal with it progressively."

One option is to slow down the syn­thesis of new pro­teins, a process that requires energy. Indeed, as we age, we pro­duce fewer new pro­teins, which explains why our capacity for learning and healing suffer as we grow old.

Since every pro­tein orig­i­nates from instruc­tions in the DNA, pro­tein syn­thesis can be slowed down by turning off par­tic­ular genes. A process called epi­ge­netic reg­u­la­tion accom­plishes the task by adding mol­e­c­ular tags on top of the genome. The pro­tein methio­nine syn­thase reg­u­lates this process. But what reg­u­lates methio­nine syn­thase? Oxidation.

"This enzyme is the most easily oxi­dized mol­e­cule in the body," said Deth, whose research on the sub­ject was recently pub­lished in the journal PLOS ONE. The senior author for the study, Christina Mura­tore, received her doc­torate in phar­ma­ceu­tical sci­ences from North­eastern in 2010.

When­ever the body is under oxida­tive stress, Deth explained, methio­nine syn­thase, or MS, stops working. He and his team hypoth­e­sized that MS plays an impor­tant reg­u­la­tory role in aging and that it might be impaired in autism, which Deth has con­nected to unchecked oxida­tive stress in pre­vious research.

To examine their hypoth­esis, the researchers looked at post­mortem human brain sam­ples across the lifespan, with sub­jects as young as 28 weeks of fetal devel­op­ment to as old as 84 years. They mea­sured the levels of a mol­e­cule called MS mRNA, which tran­scribes the genetic code for methio­nine syn­thase into actual protein.

As the sub­jects aged, their brain tissue showed lower levels of MS mRNA. But, sur­pris­ingly, the levels of the pro­tein itself remained con­stant across the lifespan.

Deth and his col­leagues sus­pect that this observed decrease in MS mRNA over our lives may act as a check in the system to save energy that we no longer have in plen­tiful supply and to slow down oxida­tive stress. "One way that the system can guard against too much pro­tein syn­thesis is to restrict the amount of mRNA," Deth said.

The team also com­pared MS pro­tein and mRNA levels between brain tissue sam­ples from autistic and nor­mally devel­oping sub­jects. Autistic brains had markedly less MS mRNA than the con­trol sam­ples but sim­ilar pro­tein levels. Addi­tion­ally, the age-​​dependent trend seen in nor­mally devel­oping brains was not mim­icked among the autistic sample.

If decreased MS mRNA does mean decreased pro­tein pro­duc­tion, it's no big deal for adults who don't need to make new pro­teins as often. But for the devel­oping brain, new pro­teins are crit­ical. "Your capacity for learning might be pre­ma­turely reduced because meta­bol­i­cally you can't afford it," Deth suggested.

While the results are pre­lim­i­nary and will ben­efit from repeated studies and more inves­ti­ga­tion, Deth's find­ings add to a growing body of evi­dence linking both aging and autism to oxida­tive stress.

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