I’ve listened to many parents and many people with autism describe their experiences. I’ve listened to them describe how and when symptoms first appear. I’ve listened to them ruminate on experiences prior to the recognition of autism, noting that autism symptoms began much earlier in some cases, but not in all. I also recognized that “autism” is a label based on behavioral—i.e. psychological—observations, but evidence indicates that autism is most likely neurological in nature. I deduced that what we call “autism” is probably many different things, with different causes, different treatments, different prognoses, and different complications.
People with autism are ?regularly lumped together and treated as a single group. But the world’s largest genetic study of the condition “shows that autism is many different diseases,” says Stanley Nelson, a professor of genetics and psychiatry at UCLA who collaborated on the investigation. “That insight should greatly enlighten how we think about autism and attempt to treat it.”
As the researchers reported last July, the mutations associated with autism fall all over the map. “If 100 different kids with autism walked into a clinic,” Nelson says, “chances are they’d have 100 different genetic aberrations.”
If this doesn’t change how autism research is conducted, then perhaps this will:
- Dr. Carla Shatz studies neuroplasticity.
- She discovered that MHC1 is an important protein in brain plasticity.
- This discovery was made, in part, because she didn’t “know” that MHC1 couldn’t possibly exist in the brain.
- You see, MHC1 is typically part of our immune response. Immune responses don’t pass beyond the blood-brain barrier in healthy brains.
- In the brain, MHC1 serves a different purpose, pruning cells as part of neuroplasticity.
- Imprecise pruning may be a key factor leading to what we call autism.
Research also indicates a connection between immune disorders and autism, and this may be the key to that connection. This might also explain the connection between autism and schizophrenia, both of which seem to involve imprecise pruning of synapses. Dr. Shatz research may lead to the ability to exert external control on how synapses are pruned, which could help people with a range of neurological challenges, from Parkinson’s to Alzheimer’s, from autism to schizophrenia, from stroke to brain injuries.
This still leaves us with the question: How much of this should we try to do? Just because we can, doesn’t mean we should. More on this next week.