Abnormal levels of lipid molecules in the brain, which can be sparked by exposure to common medications, may contribute to autism, a new study finds.
The researchers at York University in Canada found that two key neural pathways were affected by abnormal lipid levels (Wong et al., 2014).
One of the study’s authors, Professor Dorota Crawford, explains:
“We have found that the abnormal level of a lipid molecule called Prostaglandin E2 in the brain can affect the function of Wnt proteins.
It is important because this can change the course of early embryonic development.”
The study, published in the journal Cell Communication and Signaling, is a reminder that the causes of autism are both genetic and environmental.
Professor Crawford continues:
“It’s even more apparent from the recent literature that the environment might have a greater impact on vulnerable genes, particularly in pregnancy.
Our study provides some molecular evidence that the environment likely disrupts certain events occurring in early brain development and contributes to autism.”
One of the biggest challenges with autism, however, is that both the genetic and environmental causes are exceedingly complex.
This study may provide another piece in that puzzle.
Its first author, Christine Wong, said:
“Using real-time imaging microscopy, we determined that higher levels of PGE2 can change Wnt-dependent behaviour of neural stem cells by increasing cell migration or proliferation.
As a result, this could affect how the brain is organized and wired.
Moreover, we found that an elevated level of PGE2 can increase expression of Wnt-regulated genes — Ctnnb1, Ptgs2, Ccnd1, and Mmp9.”
Interestingly, all these genes have been previously implicated in various autism studies.”
Professor Crawford referred to the rise in autism is “alarming”:
“It’s 30 per cent higher than the previous estimate of 1 in 88 children, up from only two years earlier.
Perhaps we can no longer attribute this rise in autism incidence to better diagnostic tools or awareness of autism.”
Image credit: bies