• Schizophrenia linked to biological process called synaptic pruning.
    5 replies, posted
[QUOTE]Cambridge, Mass. January 26th, 2016 — A landmark study, based on genetic analysis of nearly 65,000 people, has revealed that [B]a person’s risk of schizophrenia is increased if they inherit specific variants in a gene related to “synaptic pruning” — the elimination of connections between neurons. The findings represent the first time that the origin of this devastating psychiatric disease has been causally linked to specific gene variants and a biological process.[/B] They also help explain decades-old observations: synaptic pruning is particularly active during adolescence, which is the typical period of onset for schizophrenia symptoms, and brains of schizophrenic patients tend to show fewer connections between neurons. The gene, called complement component 4 (C4), plays a well-known role in the immune system but has now been shown to also play a key role in brain development and schizophrenia risk. [B]The insight may allow future therapeutic strategies to be directed at the disorder’s roots, rather than just its symptoms.[/B][/QUOTE] [QUOTE]Over the past five years, geneticists led by the Broad Institute’s Stanley Center for Psychiatric Research and its collaborators around the world collected more than 100,000 human DNA samples from 30 different countries to locate regions of the human genome harboring genetic variants that increase the risk of schizophrenia. The strongest signal by far was on chromosome 6, in a region of DNA long associated with infectious disease, causing some observers to suggest that schizophrenia might be triggered by an infectious agent. But researchers had no idea which of the hundreds of genes in the region was actually responsible or how it acted. Based on analyses of the genetic data, McCarroll and Sekar focused on a region containing an unusual gene called complement component 4 (C4). Unlike most genes, C4 has a high degree of structural variability: different people have different numbers of copies and different types of the gene. McCarroll and Sekar developed a new molecular technique to characterize the C4 gene structure in human DNA samples. They also measured C4 gene activity in nearly 700 post-mortem brain samples. They found that the C4 gene structure (DNA) could predict the C4 gene activity (RNA) in each person’s brain – and used this information to infer C4 gene activity from genome data for 65,000 people with and without schizophrenia. These data revealed a striking correlation: patients who had particular structural forms of the C4 gene showed higher expression of that gene and, in turn, had a higher risk of developing schizophrenia.[/QUOTE] Lots more here: [url]http://www.broadinstitute.org/news/7823[/url]
strange, I thought that schizophrenia was caused by neurons being too interconnected. But this is a great discovery nevertheless.
[QUOTE=da space core;49626939]strange, I thought that schizophrenia was caused by neurons being too interconnected. But this is a great discovery nevertheless.[/QUOTE] That's Autism, if I recall correctly.
[QUOTE=Crazy Ivan;49627270]That's Autism, if I recall correctly.[/QUOTE] More along the lines of having too much white/gray matter (can't remember which) meaning more/less of your brain's neurons are covered in myelin sheaths
That's fantastic. Could this allow for tests to look for the gene variant?
As someone who has schizotypal which is constantly playing on the balancing line of schizophrenia, this is fantastic news. Never in my life would I wish something like schizophrenia on anyone. It's a horrid issue that has ran in my family for generations and has caused many problems thanks to the whole Schiz Scares in the 1930's - 1970's. With this current research, I'm hopeful that in the future when genetic therapy might become a thing, that we may be able to get rid of schizophrenia or at the very least minimize it's effects on those who are inflicted with it.
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