Alzheimer's Disease Research Today is a free monthly online journal that collates and summarizes the latest research about Alzheimer's Disease, including details on diagnosis, memory loss, heredity, treatment, medication. | ||||||||
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Glia and their cytokines in progression of neurodegeneration.Mrak RE, Griffin WS Department of Pathology, University of Arkansas for Medical Sciences, 629 South Elm Street, Room 3103, Little Rock, AR 72205, USA. A glia-mediated, inflammatory immune response is an important component of the neuropathophysiology of Alzheimer's disease, of the midlife neurodegeneration of Down's syndrome, and of other age-related neurodegenerative conditions. All of these conditions are associated with early and often dramatic activation of, and cytokine overexpression in, microglia and astrocytes, sometimes decades before pathological changes consistent with a diagnosis of Alzheimer's disease are apparent, as in patients with Down's syndrome or head injury. Brains of normal elderly individuals also often show Alzheimer-type neuropathological changes, although to a lesser degree than those seen in Alzheimer's disease itself. These normal age-related glial changes, likely a response to the normal wear and tear of the aging process, raise the threshold of glial activation and thus may explain the fact that even genetically determined Alzheimer's disease, resulting from genetic mutations such as those in beta-amyloid precursor protein and presenilins or from genetic duplication such as of chromosome 21, only shows the full manifestation of the disease decades after birth. In the more common sporadic form of Alzheimer's disease, age-related increases in glial activation and expression of cytokines may act in synergy with other genetic and acquired environmental risks to culminate in the development of disease. Published 10 January 2005 in Neurobiol Aging, 26(3): 349-54.
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