A substantial number of behaviour genetics and molecular genetics studies have confirmed the strong genetic component associated with AD/HD. Behaviour genetics investigates the contribution of genes and the environment to individual differences in behaviour. Such research traditionally examines familiality (Does ADHD run in families?) and heritability (Does ADHD get passed on ?) . Numerous family studies confirm the highly familial nature of ADHD, with first-degree relatives displaying a four to five fold risk of ADHD compared to the general population.
Twin studies and adoption studies, in addition, are necessary to ascertain whether the familial nature of ADHD is due to genes or the environment. Adopted children share genes but not the environment with their biological parents. Any similarity between these adopted children and biological parents can therefore be attributed to their shared genes. In the same way, similarities between adopted children and their adoptive parents can be attributed to the environment they share. Adoption studies have found that adoptive parents of children with ADHD display less behaviours of hyperactivity, and do better on standardized tests of attention than the biological parents, supporting the belief that ADHD has a genetic component. Twin studies have also investigated the genetic components of ADHD. When conducting twin studies, researchers consider behaviours which are highly common to identical twins to be influenced by genetics, with those common to non-identical twins to be caused by environmental factors. In reviewing the numerous twin studies on the heritability of ADHD, researchers have concluded that up to 90% of the aetiology of ADHD can be attributed to genetic factors.
Molecular genetics research of ADHD includes linkage and association studies. Linkage studies aim to pinpoint the location of individual genes responsible for a particular disease, an approach which has not been successful with ADHD, due to the multiple genes involved. However association studies in ADHD have followed a candidate gene approach, which has been very successful in identifying risk genes for ADHD. Focusing on the genes of neurotransmitter systems such as dopamine, serotonin and noradrenalin, it has identified DRD4, DRD5 and DAT1 as risk genes for ADHD. Researchers in the field of genetics are presently developing methods of combining behaviour genetics with molecular genetics research. These combined studies could, in the future, assist in the identification of specific genes implicated in ADHD, assisting the processes of diagnosis and treatment.
A substantial number of behaviour genetics and molecular genetics studies have confirmed the strong genetic component associated with ADHD. Behaviour genetics investigates the contribution of genes and the environment to individual differences in behaviour. Such research traditionally examines familiality (Does ADHD run in families?) and heritability (Does ADHD get passed on ?) . Numerous family studies confirm the highly familial nature of ADHD, with first-degree relatives displaying a four to five fold risk of ADHD compared to the general population.
Twin studies and adoption studies, in addition, are necessary to ascertain whether the familial nature of ADHD is due to genes or the environment. Adopted children share genes but not the environment with their biological parents. Any similarity between these adopted children and biological parents can therefore be attributed to their shared genes. In the same way, similarities between adopted children and their adoptive parents can be attributed to the environment they share. Adoption studies have found that adoptive parents of children with ADHD display less behaviours of hyperactivity, and do better on standardized tests of attention than the biological parents, supporting the belief that ADHD has a genetic component. Twin studies have also investigated the genetic components of ADHD. When conducting twin studies, researchers consider behaviours which are highly common to identical twins to be influenced by genetics, with those common to non-identical twins to be caused by environmental factors. In reviewing the numerous twin studies on the heritability of ADHD, researchers have concluded that up to 90% of the cause of ADHD can be attributed to genetic factors.
Molecular genetics research of ADHD includes linkage and association studies. Linkage studies aim to pinpoint the location of individual genes responsible for a particular disease, an approach which has not been successful with ADHD, due to the multiple genes involved. However association studies in ADHD have followed a candidate gene approach, which has been very successful in identifying risk genes for ADHD. Focusing on the genes of neurotransmitter systems such as dopamine, serotonin and noradrenalin, it has identified DRD4, DRD5 and DAT1 as risk genes for ADHD. Researchers in the field of genetics are presently developing methods of combining behaviour genetics with molecular genetics research. These combined studies could, in the future, assist in the identification of specific genes implicated in ADHD, assisting the processes of diagnosis and treatment.
(Ref: Hawi, Z., & Lowe, N. (2007). Molecular genetic aspects of attention deficit hyperactivity disorder. In M. Fitzgerald, M. Bellgrove & M. Gill (Eds.), Handbook of attention deficit hyperactivity disorder (pp. 129-149). West Sussex: John Wiley and Sons.)
Twin studies and adoption studies, in addition, are necessary to ascertain whether the familial nature of ADHD is due to genes or the environment. Adopted children share genes but not the environment with their biological parents. Any similarity between these adopted children and biological parents can therefore be attributed to their shared genes. In the same way, similarities between adopted children and their adoptive parents can be attributed to the environment they share. Adoption studies have found that adoptive parents of children with ADHD display less behaviours of hyperactivity, and do better on standardized tests of attention than the biological parents, supporting the belief that ADHD has a genetic component. Twin studies have also investigated the genetic components of ADHD. When conducting twin studies, researchers consider behaviours which are highly common to identical twins to be influenced by genetics, with those common to non-identical twins to be caused by environmental factors. In reviewing the numerous twin studies on the heritability of ADHD, researchers have concluded that up to 90% of the aetiology of ADHD can be attributed to genetic factors.
Molecular genetics research of ADHD includes linkage and association studies. Linkage studies aim to pinpoint the location of individual genes responsible for a particular disease, an approach which has not been successful with ADHD, due to the multiple genes involved. However association studies in ADHD have followed a candidate gene approach, which has been very successful in identifying risk genes for ADHD. Focusing on the genes of neurotransmitter systems such as dopamine, serotonin and noradrenalin, it has identified DRD4, DRD5 and DAT1 as risk genes for ADHD. Researchers in the field of genetics are presently developing methods of combining behaviour genetics with molecular genetics research. These combined studies could, in the future, assist in the identification of specific genes implicated in ADHD, assisting the processes of diagnosis and treatment.
A substantial number of behaviour genetics and molecular genetics studies have confirmed the strong genetic component associated with ADHD. Behaviour genetics investigates the contribution of genes and the environment to individual differences in behaviour. Such research traditionally examines familiality (Does ADHD run in families?) and heritability (Does ADHD get passed on ?) . Numerous family studies confirm the highly familial nature of ADHD, with first-degree relatives displaying a four to five fold risk of ADHD compared to the general population.
Twin studies and adoption studies, in addition, are necessary to ascertain whether the familial nature of ADHD is due to genes or the environment. Adopted children share genes but not the environment with their biological parents. Any similarity between these adopted children and biological parents can therefore be attributed to their shared genes. In the same way, similarities between adopted children and their adoptive parents can be attributed to the environment they share. Adoption studies have found that adoptive parents of children with ADHD display less behaviours of hyperactivity, and do better on standardized tests of attention than the biological parents, supporting the belief that ADHD has a genetic component. Twin studies have also investigated the genetic components of ADHD. When conducting twin studies, researchers consider behaviours which are highly common to identical twins to be influenced by genetics, with those common to non-identical twins to be caused by environmental factors. In reviewing the numerous twin studies on the heritability of ADHD, researchers have concluded that up to 90% of the cause of ADHD can be attributed to genetic factors.
Molecular genetics research of ADHD includes linkage and association studies. Linkage studies aim to pinpoint the location of individual genes responsible for a particular disease, an approach which has not been successful with ADHD, due to the multiple genes involved. However association studies in ADHD have followed a candidate gene approach, which has been very successful in identifying risk genes for ADHD. Focusing on the genes of neurotransmitter systems such as dopamine, serotonin and noradrenalin, it has identified DRD4, DRD5 and DAT1 as risk genes for ADHD. Researchers in the field of genetics are presently developing methods of combining behaviour genetics with molecular genetics research. These combined studies could, in the future, assist in the identification of specific genes implicated in ADHD, assisting the processes of diagnosis and treatment.
(Ref: Hawi, Z., & Lowe, N. (2007). Molecular genetic aspects of attention deficit hyperactivity disorder. In M. Fitzgerald, M. Bellgrove & M. Gill (Eds.), Handbook of attention deficit hyperactivity disorder (pp. 129-149). West Sussex: John Wiley and Sons.)
