ArticlesSerotonin transporters are preserved in the neocortex of anxious Alzheimer's disease patientsTsang, Shirley W. Y.1,3; Lai, Mitchell K. P.2,4,CA; Francis, Paul T.5; Wong, Peter T.-H.3; Spence, Ian4; Esiri, Margaret M.6; Keene, Janet7; Hope, Tony7,8; Chen, Christopher P. L.-H.1Author Information 1Neurodegenerative Diseases Program, National Neuroscience Institute; 2Department of Clinical Research, Block 6, Level 6, Room B22, Singapore General Hospital, Outram Road, Singapore 169608; 3Department of Pharmacology, National University of Singapore, Singapore 119260; 4Department of Pharmacology, University of Sydney, New South Wales 2006, Australia; 5Dementia Research Laboratory, Centre for Neuroscience Research, GKT School of Biomedical Science, King's College, London SEI IUL; 6Departments of Neuropathology; 7Psychiatry and 8Ethox, Institute of Health Sciences, University of Oxford, Oxford, UK CA,2Corresponding Author and Address: [email protected] Received 1 January 2003; accepted 3 April 2003 NeuroReport: July 18th, 2003 - Volume 14 - Issue 10 - p 1297-1300 doi: 10.1097/01.wnr.0000077546.91466.a8 Buy Metrics Abstract Densities of serotonin transporters (5-HTT) in the postmortem neocortex of behaviorally assessed Alzheimer's disease (AD) patients and aged controls were measured by radioligand binding with [3H]citalopram. It was found that 5-HTTsites in the temporal cortex of AD patients with prominent antemortem anxiety were unaltered compared with controls, but were reduced in non-anxious AD subjects. Furthermore, homozygosity for the high activity allele of a functional polymorphism in the 5-HTT gene promoter region (5-HTTLPR) was associated with both increased [3H]citalopram binding and occurrence of anxiety in the AD subjects. Since serotonin-synthesizing neurons are known to be lost in the AD cortex, this study suggests that the preservation of 5-HTT may exacerbate serotonergic deficits and underlie anxiety symptoms in AD. © 2003 Lippincott Williams & Wilkins, Inc.