| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Supplement: Living Well to 100: Nutrition, Genetics, Inflammation |
1 From the Donald W Reynolds Department of Geriatrics, The University of Arkansas for Medical Sciences, and the Geriatric Research Education Clinical Center, Central Arkansas Veterans Healthcare System, Little Rock, AR
ABSTRACT
The decline in mental fitness associated with Alzheimer disease is accompanied by physical changes in the brain, including the development of characteristic plaques and neurofibrillary tangles, but the pathogenesis of those changes is not clear. Recent work suggests that the activation of microglia in response to injury, illness, aging, or other causes begins a cascade of events that can best be characterized as an inflammatory process. This cascade is mediated at first by the proinflammatory cytokine interleukin 1, which is overexpressed by the activated microglia. Through various pathways, interleukin 1 causes neuronal death, which activates more microglia, which in turn release more interleukin 1 in a self-sustaining and self-amplifying fashion. Over a period of years, this slow, smoldering inflammation in the brain destroys sufficient neurons to cause the clinical signs of Alzheimer disease.
Key Words: Microglia • Alzheimer disease • interleukin 1 • astrocytes
This article has been cited by other articles:
|
|
 |
|
  M. C. Janelsins, M. A. Mastrangelo, K. M. Park, K. L. Sudol, W. C. Narrow, S. Oddo, F. M. LaFerla, L. M. Callahan, H. J. Federoff, and W. J. Bowers Chronic Neuron-Specific Tumor Necrosis Factor-Alpha Expression Enhances the Local Inflammatory Environment Ultimately Leading to Neuronal Death in 3xTg-AD Mice Am. J. Pathol., December 1, 2008; 173(6): 1768 - 1782. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Ramesh, J. T. Borda, J. Dufour, D. Kaushal, R. Ramamoorthy, A. A. Lackner, and M. T. Philipp Interaction of the Lyme Disease Spirochete Borrelia burgdorferi with Brain Parenchyma Elicits Inflammatory Mediators from Glial Cells as Well as Glial and Neuronal Apoptosis Am. J. Pathol., November 1, 2008; 173(5): 1415 - 1427. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. K. Anandatheerthavarada and L. Devi Amyloid Precursor Protein and Mitochondrial Dysfunction in Alzheimer's Disease Neuroscientist, December 1, 2007; 13(6): 626 - 638. [Abstract] [PDF]
|
|
|
|
 |
|
 G. Esposito, T. Iuvone, C. Savani, C. Scuderi, D. De Filippis, M. Papa, V. Di Marzo, and L. Steardo Opposing Control of Cannabinoid Receptor Stimulation on Amyloid-beta-Induced Reactive Gliosis: In Vitro and in Vivo Evidence J. Pharmacol. Exp. Ther., September 1, 2007; 322(3): 1144 - 1152. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. S. Tan, A. S. Beiser, R. S. Vasan, R. Roubenoff, C. A. Dinarello, T. B. Harris, E. J. Benjamin, R. Au, D. P. Kiel, P. A. Wolf, et al. Inflammatory markers and the risk of Alzheimer disease: The Framingham Study Neurology, May 29, 2007; 68(22): 1902 - 1908. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. B. Rowe, E. M. Blalock, K.-C. Chen, I. Kadish, D. Wang, J. E. Barrett, O. Thibault, N. M. Porter, G. M. Rose, and P. W. Landfield Hippocampal Expression Analyses Reveal Selective Association of Immediate-Early, Neuroenergetic, and Myelinogenic Pathways with Cognitive Impairment in Aged Rats J. Neurosci., March 21, 2007; 27(12): 3098 - 3110. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Stasi, D. Nagel, X. Yang, L. Ren, T. Mittag, and J. Danias Ceruloplasmin Upregulation in Retina of Murine and Human Glaucomatous Eyes Invest. Ophthalmol. Vis. Sci., February 1, 2007; 48(2): 727 - 732. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
