There is a paper in the latest issue of Nature that spells the development of a new perspective on schizophrenia. The paper by Aswin Sekar and others identifies the genetic risks for schizophrenia.
It was well known that the Major Histocompatibility Complex (MHC), the genetic system that forms the basis for the distinguishing of self and the other by the immune system, has a strong association with schizophrenia. But the genes and molecular mechanisms for this had not been identified. The recent paper in Nature does exactly that.
There are many structurally diverse alleles of the complement component 4 (C4) genes of the Major Histocompatibility Complex in Chromosome 6. These alleles produce widely varying levels of C4A and C4B proteins in the brain. In schizophrenia, there is more of the C4A protein.
The C4 proteins are localized mainly in neuronal synapses, dendrites, axons, and cell bodies. They are responsible for synapse elimination during postnatal development. The over expression of C4A proteins thus explains the reduced numbers of synapses in the brains of individuals with schizophrenia.
The findings are significant since now one can focus on genetically modifying the expression of the C4A allele. I predict that there will be more papers in this direction this year itself.
It was well known that the Major Histocompatibility Complex (MHC), the genetic system that forms the basis for the distinguishing of self and the other by the immune system, has a strong association with schizophrenia. But the genes and molecular mechanisms for this had not been identified. The recent paper in Nature does exactly that.
There are many structurally diverse alleles of the complement component 4 (C4) genes of the Major Histocompatibility Complex in Chromosome 6. These alleles produce widely varying levels of C4A and C4B proteins in the brain. In schizophrenia, there is more of the C4A protein.
The C4 proteins are localized mainly in neuronal synapses, dendrites, axons, and cell bodies. They are responsible for synapse elimination during postnatal development. The over expression of C4A proteins thus explains the reduced numbers of synapses in the brains of individuals with schizophrenia.
The findings are significant since now one can focus on genetically modifying the expression of the C4A allele. I predict that there will be more papers in this direction this year itself.
Aswin Sekar et. al. Schizophrenia risk from complex variation of complement component 4,
Nature (2016) doi:10.1038/nature16549
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