Systemic and acquired immune responses in Alzheimer's disease.
Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by a progressive cognitive decline and dementia. AD brains are marked by amyloid plaques and neurofibrillary tangles, neuronal cell loss, and a prominent activation of glial cells, and innate immune responses. A growing number of studies in AD have also reported alterations in systemic immune responses including changes in lymphocyte and macrophage distribution and activation, the presence of autoantibodies, or abnormal cytokine production. Studies in animal models for AD support the notion that immune cells infiltrate the brain and may modulate the disease. Here we will review evidence for systemic alterations in immune responses and a role for acquired immunity in AD and discuss their potential contribution to the disease.
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.
Markus
M
Britschgi
Tony
T
Wyss-Coray
D000544:Alzheimer Disease / Q000276:immunology* / Q000473:pathology*; D000818:Animals; D000917:Antibody Formation / Q000502:physiology; D006801:Humans; D007111:Immunity, Cellular / Q000502:physiology; D008214:Lymphocytes / Q000276:immunology / Q000502:physiology; D008264:Macrophages / Q000276:immunology / Q000502:physiology; D009000:Monocytes / Q000276:immunology / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000096:biosynthesis
D009419:Nerve Tissue Proteins