|Understanding ADHD Inattentive and Aging|
One of the things that fascinates me the most is the fact that I seemed to have, at some point, "out grown" many of my symptoms. As I aged my inattention improved, my organizational skills improved, my anxiety improved, my introversion improved, my reading improved and my analytic skill improved. I have thought that these improvements have had to do with many positive things occurring in my life (coffee,exercise, an improved diet, continued family support) but I have also thought that the main thing that happened to me is that my brain "grew up".
When I read a study like the one copied below it gets me thinking again about the role of aging and inattentive ADHD symptoms. I am totally unfamiliar with SLC9A9, with the solute carrier family , with Na+/H+ exchanger, with NHE9 and, for that matter, with membrane proteins that regulates luminal pH of endosomes but there is a sentence in this abstract that is interesting to me, "We observed an age-dependent abnormal expression of SLC9A9 in brains of this inattentive model". Now granted this is a rat study but other studies have shown that the Inattentive rat can be a good sample to study the brain's of people with the Inattentive type of ADHD.
The authors report that the SLC9A9 protein is essential for proper synaptic transmission and proper brain plasticity and it appears that they found the abnormality to be age dependent. It is unclear if the abnomalities improve or worsen with age but the fact that these changes are age dependent are interesting to me. Aging changes our brain and it sometimes does so for the better. In the old days, ADHD was considered to be a disorder of delayed brain development. Adults were expected to improve either because they learned to manage their symptoms of because their symptoms, as I believe happened to me, improved.
What do you think? How have your ADHD symptoms changed with age. I would love to hear from you.
Am J Med Genet B Neuropsychiatr Genet. 2011 Aug 19. doi: 10.1002/ajmg.b.31229. [Epub ahead of print]
SLC9A9 mutations, gene expression, and protein-protein interactions in rat models ofattention-deficit/hyperactivity disorder.
Department of Psychiatry, SUNY Upstate Medical University, Syracuse, New York.
SLC9A9 (solute carrier family 9, member 9, also known as Na+/H+ exchanger member (NHE9)) is a membrane protein that regulates the luminal pH of the recycling endosome, an essential organelle for synaptic transmission and plasticity. SLC9A9 has been implicated in human attention deficit hyperactivity disorder (ADHD) and in rat studies of hyperactivity. We examined the SLC9A9 gene sequence and expression profile in prefrontal cortex, dorsal striatum and hippocampus in two genetic rat models of ADHD. We report two mutations in a rat model of inattentive ADHD, the WKY/NCrl rat, which affect the interaction of SLC9A9 with calcineurin homologous protein (CHP). We observed an age-dependent abnormal expression of SLC9A9 in brains of this inattentive model and in the Spontaneous Hypertensive Rat (SHR) model of ADHD. Our data suggest a novel mechanism whereby SLC9A9 sequence variants and abnormalities in gene expression could contribute to the ADHD-like symptoms of rat models and possibly the pathophysiology of ADHD in humans.