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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kim, Jungsu Sheline, Yvette I. Sathyan, Anshul Verges, Deborah K. Benzinger, Tammie Mintun, Mark A. Restivo, Jessica L. Morris, John C. Cirrito, John R. D'angelo, Gina Yoon, Hyejin Hayreh, Davinder Disabato, Brianne M. Goebel, Whitney D. |
| Description | Author Affiliation: Cirrito JR ( Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA. cirritoj@neuro.wustl.edu); |
| Abstract | Aggregation of amyloid-ß (Aß) as toxic oligomers and amyloid plaques within the brain appears to be the pathogenic event that initiates Alzheimer's disease (AD) lesions. One therapeutic strategy has been to reduce Aß levels to limit its accumulation. Activation of certain neurotransmitter receptors can regulate Aß metabolism. We assessed the ability of serotonin signaling to alter brain Aß levels and plaques in a mouse model of AD and in humans. In mice, brain interstitial fluid (ISF) Aß levels were decreased by 25% following administration of several selective serotonin reuptake inhibitor (SSRI) antidepressant drugs. Similarly, direct infusion of serotonin into the hippocampus reduced ISF Aß levels. Serotonin-dependent reductions in Aß were reversed if mice were pretreated with inhibitors of the extracellular regulated kinase (ERK) signaling cascade. Chronic treatment with an SSRI, citalopram, caused a 50% reduction in brain plaque load in mice. To test whether serotonin signaling could impact Aß plaques in humans, we retrospectively compared brain amyloid load in cognitively normal elderly participants who were exposed to antidepressant drugs within the past 5 y to participants who were not. Antidepressant-treated participants had significantly less amyloid load as quantified by positron emission tomography (PET) imaging with Pittsburgh Compound B (PIB). Cumulative time of antidepressant use within the 5-y period preceding the scan correlated with less plaque load. These data suggest that serotonin signaling was associated with less Aß accumulation in cognitively normal individuals. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 36 |
| Volume Number | 108 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2011-09-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Alzheimer Disease Drug Therapy Amyloid Beta-Peptides Metabolism Antidepressive Agents, Second-Generation Administration & Dosage Brain Citalopram Serotonin Signal Transduction Drug Effects Genetics Aniline Compounds Animals Mice Mice, Transgenic Positron-Emission Tomography Radiography Thiazoles Time Factors Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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