The Study Of Circulation Glutamate, Aβ_1-40 And Aβ_1-42 Levels In Patients With Acute Ischemic Stroke

ObjectiveAcute ischemic stroke(AIS) damage represents a major source of morbidity and mortality in society. Despite of advances in acute and prophylactic therapies,to date, few effective therapies have been realized to treat stroke and once promising avenues have not proven clinically useful. Glutamate(Glu) is the main excitatory neurotransmitter in the central nervous system(CNS).Neuronal death induced by most Glu release and overactive Glu receptor after ischemia stroke. In the brains of Alzheimer's disease patients amyloid beta-peptide(Aβ) is the major component of senile plaque. Aβis formed by sequential breakdown ofβamyloid precursor protein(βAPP). Cleavage ofβAPP by -secretase results in the production of the Aβ1–40 and Aβ1–42. Including the neurotoxicity induced by Aβstraightly or indirectly ,recent studies suggested that Aβmight be an important steady substance involved in the process of nerve excitation in the CNS. The potentially synergistic multiple effects of Aβon Glu function, including enhancing its release, preventing its uptake, and increasing neuronal vulnerability .There may be some correlations between Aβand Glu in patients with acute ischemic stroke.But the correlations have not been kown clearly.Thus we investigate the changes and clinical implications of blood Aβ1–40 ,Aβ1–42 and Glu levels and the prognosis in patients with acute ischemic stroke.MethodsWe prospectively enrolled 27 patients with acute ischemic stroke and 11 age-matched controls to detect the serum Glu,Aβ1-40 and plasma Aβ1-42 (at admission and one week after admission). The blood Aβlevels were...