Inflammation in Alzheimer disease-a brief review of the basic science and clinical literature.
Biochemical and neuropathological studies of brains from individuals with Alzheimer disease (AD) provide clear evidence for an activation of inflammatory pathways, and long-term use of anti-inflammatory drugs is linked with reduced risk to develop the disease. As cause and effect relationships between inflammation and AD are being worked out, there is a realization that some components of this complex molecular and cellular machinery are most likely promoting pathological processes leading to AD, whereas other components serve to do the opposite. The challenge will be to find ways of fine tuning inflammation to delay, prevent, or treat AD.
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305-5235, USA; Geriatric Research Education and Clinical Center, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304, USA.
Tony
T
Wyss-Coray
Joseph
J
Rogers
D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology* / Q000517:prevention & control; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D016718:Arachidonic Acid / Q000378:metabolism; D001253:Astrocytes / Q000473:pathology; D002986:Clinical Trials as Topic; D003167:Complement Activation / Q000502:physiology; D003165:Complement System Proteins / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D004660:Encephalitis / Q000473:pathology*; D006801:Humans; D051379:Mice; D017628:Microglia / Q000473:pathology; D009474:Neurons / Q000473:pathology; D009836:Oligodendroglia / Q000473:pathology; D011110:Polymorphism, Genetic / Q000235:genetics; D011451:Prostaglandin-Endoperoxide Synthases / Q000502:physiology; D051193:Toll-Like Receptors / Q000502:physiology
D000893:Anti-Inflammatory Agents; D016207:Cytokines; D051193:Toll-Like Receptors; D016718:Arachidonic Acid; D003165:Complement System Proteins; D011451:Prostaglandin-Endoperoxide Synthases