Neural bases for the visual lexicon and for auditory verbal short-term memory components have been proposed, with some implication that the observed neural manifestation of developmental dyslexia is task-specific (i.e., functional rather than structural). fMRIs of people with dyslexia indicate an interactive role of the cerebellum and cerebral cortex as well as other brain structures in reading.The cerebellar theory of dyslexia proposes that impairment of cerebellum-controlled muscle movement affects the formation of words by the tongue and facial muscles, resulting in the fluency problems that some people with dyslexia experience. The cerebellum is also involved in the automatization of some tasks, such as reading. The fact that some children with dyslexia have motor task and balance impairments could be consistent with a cerebellar role in their reading difficulties. However, the cerebellar theory has not been supported by controlled research studies. Genetics
Research into potential genetic causes of dyslexia has its roots in post-autopsy examination of the brains of people with dyslexia. Observed anatomical differences in the language centers of such brains include microscopic cortical malformations known as ectopias, and more rarely, vascular micro-malformations, and microgyrus—a smaller than usual size for the gyrus. The previously cited studies and others suggest that abnormal cortical development, presumed to occur before or during the sixth month of fetal brain development, may have caused the abnormalities. Abnormal cell formations in people with dyslexia have also been reported in non-language cerebral and subcortical brain structures.
This disruption to the electrochemical gradient is in part rectified by the passive secretion of positively charged sodium ions in to the lumen and water follows by osmosis.Plecanatide is also known to have an anti-nociceptive effect in animal models, however the exact mechanism of action is not yet fully elucidated. It has been suggested that this may be in part to the anti-inflammatory action of guanylate cyclase-C by its inhibition of pro-inflammatory cytokines, or through the inhibition of associated sensory neurons. Pharmacokinetics and metabolism
As plecanatide acts on receptors present on the apical side of endothelial cells lining the gastrointestinal tract it is able to impart its effect without ever entering circulation. As with most orally ingested peptides, plecanatide is degraded by intestinal enzymes, and so very little of the active drug enters systemic circulation. Minimal amounts of the drug are expected to be transported in to the body, and concentrations of plecanatide and its metabolites are undetectable in plasma following the recommended dosage of 3 mg. It has also been shown that dosages up to 48.6 mg produced no detectable concentration of plecanatide in human plasma at any time point after ingestion. References
External links
"Plecanatide". Drug Information Portal. U.S. National Library of Medicine.