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The Journal of Neuroscience, April 26, 2006, 26(17):4644-4648; doi:10.1523/JNEUROSCI.4822-05.2006

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Brief Communications
-Amyloid Stimulates Murine Postnatal and Adult Microglia Cultures in a Unique Manner

Angela M. Floden and Colin K. Combs

Department of Pharmacology, Physiology, and Therapeutics, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota 58202

Correspondence should be addressed to Dr. Colin K. Combs, Department of Pharmacology, Physiology, and Therapeutics, School of Medicine and Health Sciences, University of North Dakota, 504 Hamline Street, Neuroscience Building, Grand Forks, ND 58202. Email: ccombs{at}medicine.nodak.edu

Reactive microglia are commonly observed in association with the -amyloid (A) plaques of Alzheimer's disease brains. This localization supports the hypothesis that A is a specific activating stimulus for microglia. A variety of in vitro studies have used postnatal derived rodent microglia cultures to characterize the ability of A to stimulate these cells. However, it is unclear whether this paradigm accurately models conditions in aged animals. To determine whether A stimulatory phenotypes differ between young and adult microglia, we established cultures of acutely isolated adult murine cortical microglia to compare with postnatal derived microglial cultures. Although cells from both ages expressed robust immunoreactivity for CD68 and CD11b, their responses to activating stimuli differed. Fibrillar A was rapidly phagocytosed by postnatal microglia and both oligomeric and fibrillar peptide stimulated increased tumor necrosis factor (TNF) secretion. However, A oligomers but not fibrils stimulated TNF secretion from adult microglia. More importantly, adult microglia had diminished ability to phagocytose A fibrils. These findings demonstrate that adult microglia respond to A fibril stimulation uniquely from postnatal cells and suggest that adult rather than postnatal microglia cultures are more appropriate for modeling proinflammatory changes in the aged CNS.

Key words: microglia; tumor necrosis factor; A; peptide; amyloid; neuroinflammation; Alzheimer

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Received Nov. 9, 2005; revised March 6, 2006; accepted March 29, 2006.

Correspondence should be addressed to Dr. Colin K. Combs, Department of Pharmacology, Physiology, and Therapeutics, School of Medicine and Health Sciences, University of North Dakota, 504 Hamline Street, Neuroscience Building, Grand Forks, ND 58202. Email: ccombs{at}medicine.nodak.edu

This article has been cited by other articles:

				M. Jana, C. A. Palencia, and K. Pahan Fibrillar Amyloid-{beta} Peptides Activate Microglia via TLR2: Implications for Alzheimer's Disease J. Immunol., November 15, 2008; 181(10): 7254 - 7262. [Abstract] [Full Text] [PDF]

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