Although heredity has been implicated in over 80% of Autism and Schizophrenia and Bipolar disorder cases, no single gene or cluster of genes has stood out to be the culprit or cause for these disorders. Genes are normally present as a single entity on a chromosome strand. Sometimes, more than one copy of a gene on a strand may be present. The copy number of genes that encode for proteins neurexins and neuroligin are variable and likely to be present in some individuals who have autism or schizophrenia. However, they may not be the cause of autism or schizophrenia in every individual carrying a copy number variation of these genes. This complicates research. Another external factor has to be the “triger” which when present (could it be an environmental toxin or perhaps a bout of gastroenteritis during a MMR vaccine shot or an unknown factor/s) along with a variable copy number of neurexin or neuroligin gene may result in an autistic child or a schizophrenic individual.
There is strong evidence that genetic factors make substantial contributions to the etiology of autism, schizophrenia and bipolar disorders, with heritability estimates being at least 80% for each. These illnesses have complex inheritance, with multiple genetic and environmental factors influencing disease risk; however, in psychiatry, complex genetics is further compounded by phenotypic complexity. Autism, schizophrenia and bipolar disorder are effectively syndromic constellations of symptoms that define groups of patients with broadly similar outcomes and responses to treatment. As such the diagnostic categories are likely to be heterogeneous and the boundaries between them somewhat arbitrary. Recent applications of whole-genome technologies have discovered rare copy number variants and common single-nucleotide polymorphisms that are associated with risk of developing these disorders. Furthermore, these studies have shown an overlap between the genetic loci and even alleles that predispose to the different phenotypes. The findings have several implications. First, they show that copy number variations are likely to be important risk factors for autism and schizophrenia, whereas common single-nucleotide polymorphism alleles have a role in all disorders. Second, they imply that there are specific genetic loci and alleles that increase an individual’s risk of developing any of these disorders. Finally, the findings suggest that some of the specific genetic loci implicated so far encode proteins, such as neurexins and neuroligins, that function in synaptic development and plasticity, and therefore may represent a common biological pathway for these disorders.
One cannot help wondering naturally, if Autism and Schizophrenia can be prevented. With more research on genetics and environment or trigger, with a lot of public help. What kind of help? If the research community joined the public community to form a scientific table of exposures and gene copy variation and family occupations and bouts of gastroenteritis a few months before or after vaccination and toxic spill near home community or home built on previously heavily fertilized agricultural land or father working in a pesticide or herbicide exposed occupation or home lawn heavily sprayed with a pesticide or herbicide or community water exposed to run-off from pesticide and herbicide or a toxic dump site and so much more. Science research is not funded enough to recruit large scale public help or to inspire large community assistance. Together we can tackle this scourge and prevent future cases of Autism, and perhaps Schizophrenia. Inspire your community to encourage scientists to join in a larger than ever world-wide community to volunteer information in a legitimate manner that can be scientifically analyzed. Together we can do it!
A journal article published in Genome Medicine 2009, 1:102 by Liam S Carroll and Michael J Owen, which you may click here to read, researchers the genetics in detail described above. An excerpt is quoted below.
It has long been recognized that psychiatric disorders and symptoms aggregate in families and the evidence for a substantial role for genetic factors is incontrovertible . Genetic epidemiological studies of autism, bipolar disorder and schizophrenia show that the risk of developing one of these specific psychiatric illnesses is proportional to the amount of genetic material shared with an affected individual . Heritability has been estimated as being at least 80% for all these disorders [2–4], which, to put it in context, is equivalent to that for type I diabetes (about 80%)  but greater than that for breast cancer  or Parkinson’s disease .