No Evidence of Endothelial Dysfunction in Patients with Alzheimer’s Disease

• Published in: Dementia and geriatric cognitive disorders Vol. 11; no. 4; pp. 197 - 201
• Main Authors: McGleenon, B.M., Passmore, A.P., McAuley, D.F., Johnston, G.D.
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland Karger 01.07.2000; S. Karger AG
• Subjects: Acetylcholine - administration & dosage; Acetylcholine - pharmacology; Aged; Aged, 80 and over; Alzheimer Disease - complications; Alzheimer Disease - physiopathology; Biological and medical sciences; Brachial Artery - drug effects; Case-Control Studies; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Dose-Response Relationship, Drug; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiopathology; Female; Forearm - blood supply; Humans; Infusions, Intra-Arterial; Male; Medical sciences; Middle Aged; Neurology; Nitroprusside - administration & dosage; Nitroprusside - pharmacology; Original Research Article; Plethysmography - methods; Regional Blood Flow - drug effects; Vascular Diseases - complications; Vascular Diseases - physiopathology; Vasodilator Agents - pharmacology; Pathogenesis; Alzheimer's disease; Systemic effect; Vascular pathology; Human; Regional blood flow; Nervous system diseases; Alzheimer disease; Exploration; Cerebral disorder; Endothelium; Forearm; Blood vessel; Central nervous system disease; Degenerative disease; Circulatory system; Hemodynamics; Elderly
• ISSN: 1420-8008; 1421-9824
• DOI: 10.1159/000017237

In view of accumulating evidence of vascular pathology in Alzheimer’s disease (AD), we tested the hypothesis that AD patients have impaired endothelial function. This was assessed using the technique of strain-gauge venous occlusion plethysmography, which measures forearm blood flow (FBF). Intra-arterial (brachial) infusion of acetylcholine (ACh) and sodium nitroprusside (SNP) was used to assess local endothelial dependent and independent responses, respectively. There was no difference in the basal FBF of patients and controls. ACh and SNP caused dose-related increases in FBF from baseline, but no difference was recorded between the AD and control group. This study provides no evidence of endothelial dysfunction in the systemic circulation of patients with AD.