Anti-inflammatory actions of peroxisome proliferator-activated receptor gamma agonists in Alzheimer’s disease
The role of inflammatory processes in the brains of Alzheimer’s Disease (AD) patients has recently attracted considerable interest. Indeed, the only demonstrated effective therapy for AD patients is long-term treatment with non-steroidal anti-inflammatory drugs (NSAIDs). The mechanistic basis of the...
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| Veröffentlicht in: | Neurobiology of aging 2001-11, Vol.22 (6), p.937-944 |
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| container_title | Neurobiology of aging |
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| creator | Landreth, Gary E Heneka, Michael T |
| description | The role of inflammatory processes in the brains of Alzheimer’s Disease (AD) patients has recently attracted considerable interest. Indeed, the only demonstrated effective therapy for AD patients is long-term treatment with non-steroidal anti-inflammatory drugs (NSAIDs). The mechanistic basis of the efficacy of NSAIDs in AD remains unclear. However, the recent recognition that NSAIDs can bind to and activate the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), has offered an explanation for the action of these drugs in AD. PPARγ activation leads to the inhibition of microglial activation and the expression of a broad range of proinflammatory molecules. The newly appreciated anti-inflammatory actions of PPARγ agonists may allow novel therapies for AD and other CNS indications with an inflammatory component. |
| doi_str_mv | 10.1016/S0197-4580(01)00296-2 |
| format | Article |
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Indeed, the only demonstrated effective therapy for AD patients is long-term treatment with non-steroidal anti-inflammatory drugs (NSAIDs). The mechanistic basis of the efficacy of NSAIDs in AD remains unclear. However, the recent recognition that NSAIDs can bind to and activate the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), has offered an explanation for the action of these drugs in AD. PPARγ activation leads to the inhibition of microglial activation and the expression of a broad range of proinflammatory molecules. 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Indeed, the only demonstrated effective therapy for AD patients is long-term treatment with non-steroidal anti-inflammatory drugs (NSAIDs). The mechanistic basis of the efficacy of NSAIDs in AD remains unclear. However, the recent recognition that NSAIDs can bind to and activate the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), has offered an explanation for the action of these drugs in AD. PPARγ activation leads to the inhibition of microglial activation and the expression of a broad range of proinflammatory molecules. 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| ispartof | Neurobiology of aging, 2001-11, Vol.22 (6), p.937-944 |
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| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Alzheimer Disease - pathology Alzheimer Disease - prevention & control Alzheimer’s disease Animals Anti-Inflammatory Agents, Non-Steroidal - pharmacology Cyclooxygenases Humans Inflammation Inflammation - prevention & control Microglia NSAIDs Peroxisome proliferator-activated receptors Receptors, Cytoplasmic and Nuclear - agonists Receptors, Cytoplasmic and Nuclear - biosynthesis Receptors, Cytoplasmic and Nuclear - physiology Transcription Factors - agonists Transcription Factors - biosynthesis Transcription Factors - physiology |
| title | Anti-inflammatory actions of peroxisome proliferator-activated receptor gamma agonists in Alzheimer’s disease |
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