Skip to main content

What About Us?

It’s been almost two decades since the discovery that alterations in MECP2 cause Rett Syndrome. However, the diagnosis of Rett remains a clinical one based on a child’s symptoms and history. While a positive MECP2 genetic test confirms the diagnosis, it is not required. This creates a situation where individuals can have a diagnosis of Rett without an MECP2 alteration and conversely, individuals can have an MECP2 alteration but not fit the symptomatic criteria for Rett Syndrome and therefore not have a clinical diagnosis.

With our recent Roadmap to a Cure launch and its emphasis on curative approaches that target MECP2 as well as the AveXis gene therapy announcement, I am hearing increasingly from parents whose children don’t have an MECP2 alteration. They are understandably asking, “What about us? Where does this progress leave my child?” The answer to those questions is that a confirmed MECP2 alteration will be a “must have” for any future interventions that target MECP2. So having an MECP2 alteration will be part of the inclusion criteria for gene therapy trials as well as any other interventions that target this gene.

I know parents will agree that having a Rett clinical diagnosis without being able to take advantage of any gene-specific interventions is extremely frustrating. Getting to the root of your child’s symptoms is extremely important.
Towards that end I would recommend the following:

1. Make sure that the MECP2 testing that was done included not only sequencing but also large exonic deletions (also called MLPA testing). The testing is usually done in a two-step process. If the sequencing comes back negative then the exonic deletion testing should be pursued. This doesn’t usually happen automatically as it needs to be ordered and paid for. Furthermore, exonic deletion testing for MECP2 became routinely available about 10 years ago, so if your child was tested before then you might want to revisit this.

2. MECP2 testing that was done in the early days did not include exon 1. Although mutations in exon 1 are rare it is certainly worth checking. Check your child’s genetic results and see if exon 1 was included. If you don’t have the genetic results, ask for them. It’s important that you know exactly what was done. If you are unsure how to read the results feel free to email them to me – I’m happy to take a look.

3. If sequencing (exons 1 through 4) and MLPA testing is negative you may want to explore redoing the testing. Although a rarity, mistakes can sometimes happen and rechecking would rule out this possibility.

4. Another rarity is sporadic mutations that arise post-conception in a single cell as an embryo is forming as opposed to mutations that come from the germ line (sperm or egg). When this occurs any daughter cells that are generated from the mutated cell will also have the mutation. But there will be many other cells that are normal. This scenario may be missed by traditional sequencing and may require more detailed testing, which should be discussed with a geneticist.

5. If the above testing confirms that your child doesn't have alterations in MECP2 then it’s time to look beyond this gene. First ensure that mutations in genes like CDKL5, FOXG1, UBE3A, TCF4 have been ruled out. Mutations in these genes can cause Rett-like symptoms.

6. Next explore whole genome or whole exome sequencing (the protein producing section of the genome). While there is no guarantee that anything will be identified, the “hit rates” are getting better and better.

If you feel that you are hitting a brick wall regarding the steps outlined above feel free to email me, I may be able to provide some help. The field of genetics is evolving rapidly with discoveries being made daily. A yearly visit to a geneticist is definitely worthwhile.

My heart goes out to parents who find themselves in limbo due to a lack of a clear diagnosis. Please don’t give up. Technological and analytical improvements bode well. I have no doubt that in time you will have your answer.

In the meantime please know that much of the research we are supporting, such as the gene therapy work, will provide information and data that will be useful for other neurological disorders as well.