Attenuation of Aβ deposition in the entorhinal cortex of normal elderly individuals associated with tobacco smoking

摘要: Investigating correlates of tobacco smoking provides the only currently available opportunity examining effects long-term exposure nicotinic receptors on a specific agonist in human. Alzheimer-type pathology (Abeta and abnormally phosphorylated tau assessed basis AT8 immunoreactivity) together with vascular markers has been compared age-matched groups normal elderly smokers non-smokers entorhinal cortex, an area noted age-related pathology. The density total Abeta diffuse immunoreactivity, formic acid-extractable Abeta42 but not Abeta40, was reduced (n = 10-18) 10-20) (P < 0.05). There also percentage cortical leptomeningeal vessels associated immunoreactivity 13) 14) 0.005 0.05, respectively). significant inverse correlation between pack years 34, r -0.389, P 0.025), similar trend for which did reach statistical significance 30, -0.323, 0.082). In contrast, there were no group differences (collagen IV, alpha-actin or glucose transporter 1), phosphate-buffered saline-soluble peptides, associations gender any measured parameters. These findings are consistent previously reported reductions histologically amyloid plaques aged human brain use dramatic lessening deposits APPsw mice after nicotine treatment. Development drugs to protect against beta-amyloidosis as one principal pathological hallmarks ageing Alzheimer's disease is indicated.