title: Treating asthma as a neuroelectrical disorder.
abstract: The trend in asthma therapy for the last two decades has been based on the suppression of inflammation and bronchodilation via adrenergic agonism or cholinergic antagonism. These strategies help to control asthmatic symptoms but do not lead to a cure. Substantial populations of patients may still have poorly managed symptoms and suffer a decline in quality of life due to the disease. Reversible airflow obstruction and nonspecific airway reactivity are the key features of asthma. Inflammatory changes do not correlate always with symptoms in asthma patients. It is our opinion that the primary defect in asthma is cell membrane excitation-bronchoconstriction and reactivity-rather than inflammation. Our research, clinical experience and the accumulated evidence from medical literature strongly suggest that controlling other excitatory mechanisms such as voltage-gate sodium channel and glutamate receptors in the central nervous system and lung tissue could lead to more effective and safer strategies for asthma prevention and treatment.
authors.affiliation: Allergy Research Group, Inc., Alameda, CA 95117, USA.
authors.forename: Ba X
authors.initials: BX
authors.lastname: Hoang
authors.forename: D Graeme
authors.initials: DG
authors.lastname: Shaw
authors.forename: Phuong
authors.initials: P
authors.lastname: Pham
authors.forename: Stephen A
authors.initials: SA
authors.lastname: Levine
mesh_terms: D001249:Asthma / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology* / Q000517:prevention & control; D016084:Bronchoconstriction / Q000187:drug effects; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D008168:Lung / Q000502:physiology / Q000503:physiopathology*; D008564:Membrane Potentials; D017470:Receptors, Glutamate / Q000378:metabolism; D015222:Sodium Channels / Q000378:metabolism
chemical_list: D017470:Receptors, Glutamate; D015222:Sodium Channels; D018698:Glutamic Acid