Jing Yi, Laura L. Horky, Avi L. Friedlich, Ying Shi, Jack T. Rogers, and Xudong Huang
Neurochemistry Laboratory, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA; Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; and Conjugate and Medicinal Chemistry Laboratory, Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Received 28 August 2008; Accepted 10 September 2008; Available online 2 October 2008
Abstract: Alzheimer’s disease (AD), the most common form of dementia, is characterized by progressive neurodegeneration and loss of cognitive and memory functions. Although the exact causes of AD are still unclear, evidence suggests that atherosclerosis, redox stress, inflammation, neurotransmitter dysregulation, and impaired brain energy metabolism may all be associated with AD pathogenesis. Herein, we explore a possible role for L-arginine (L-arg) in AD, taking into consideration known functions for L-arg in atherosclerosis, redox stress and the inflammatory process, regulation of synaptic plasticity and neurogenesis, and modulation of glucose metabolism and insulin activity. L-arg, a precursor of nitric oxide (NO) and polyamine, exhibits multiple functions in human health and may play a prominent role in age-related degenerative diseases such as AD. (IJCEP808005 ).
Address all correspondence to: Xudong Huang, Ph.D., Conjugate and Medicinal Chemistry Laboratory, Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.; Tel: (617) 582-4711; Fax: (617)582-0004; E-mail: xhuang3@partners.org.