The more we’ve come to appreciate these genetic and molecular mechanisms, of early cell function, differentiation, maturation, and neural system function to brain, the more we’ve actually come to question what psychiatric illness really is. Is it actually diseases, in the traditional sense of a disease like Alzheimer’s disease or heart disease or pulmonary disease?
Or are these conditions states of brain maturation function based on alterations in genes that are important for these early programs of cell growth, development, maturation, modulation, and brain function?
And we’ve increasingly come to appreciate that the genetics of psychiatric illness is the genetics of brain development and brain function. Now, these psychiatric illnesses overlap in many ways with other developmental disorders, including intellectual deficiency. But certainly the psychiatric disorders which involve maybe some similar genes and some similar mechanisms of how the early circuitry of the brain is laid out.
The noise issues that are introduced into these programs are much less severe than they are in mental deficiency or even in autism. Those are more severe disruptions of the signal that has to accumulate in a sort of lawful way in the development of these neural systems.
In psychiatric illness, the noise is probably much less considerable than it is in these more profound disorders. But there’s in many ways, at the molecular, developmental, and genetic level, these are continuums of relative noise in these early programs.
Now, many people think about these early developmental factors and get discouraged about how could you remediate these things that are happening from very early on in life. We’re not discouraged; we’re actually very encouraged by this, because what we’ve come to realize in modern molecular neurobiology over the last twenty years is that the same molecules that build a connection between neurons sustain that connection, maintain that connection, and continue to modify the connection.
These are not static, fixed, immutable molecular characteristics of human brain function. They are continually modifiable. So there’s no reason to believe necessarily that just because the mischief that some of this molecular noise—based on the genetic predispositions—have to do with early patterning of brain circuitry, are there from early in life, does not mean that we cannot somehow refocus, or redirect, or re-compensate for any of these early changes.
So I think one of the things we’ve learned now with some of these mouse models of much more profound mental difficulties like mental deficiency, the syndromes—Rett’s syndrome, Fragile-X syndrome, which is an autism related syndrome—is that these early developmental problems that are quite dramatic at the level of brain anatomy and brain development, are reversible.
They’re reversible in ways that nobody, ten years ago, imagined you could undo this early developmental change. So there’s no reason to believe that having these insights, and understanding how the risk factors, genetic and non-genetic, how the risk factors for psychiatric illness—schizophrenia in particular, which is the main focus of the Lieber Institute—how these risk factors create a, set the stage for the later problems that these brains manifest, could still be remediable, even if they’re very early in development.
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