Potential inflammatory biomarkers in Alzheimer's disease.
The role of the brain's innate immune system in Alzheimer pathogenesis is now well established. Proinflammatory cytokines elaborated by this system, in particular activated microglia-derived interleukin-1 (IL-1), drive a cascade of neurotoxic changes that are important for the development and progression of both the neuritic plaques and neurofibrillary tangles characteristic of Alzheimer's disease. Cytokine expression may also be modulated by variants of genes. For instance, inheritance of certain IL-1 gene variants is associated with Alzheimer's disease. The potential for using blood levels of proinflammatory cytokines as biomarkers of disease progression, however, remains unrealized. The interpretation of cytokine levels in the blood is complicated by the fact, for example, that the overexpression of IL-1 in Alzheimer brain may act to increase adrenal cortisol production through the hypothalamic-pituitary-adrenal axis, which acts to limit macrophage activation and peripheral cytokine production.
Mrak
Robert E
RE
Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Griffin
W Sue T
WS
D000544:Alzheimer Disease / Q000134:cerebrospinal fluid*; D015415:Biomarkers / Q000378:metabolism*; D002097:C-Reactive Protein / Q000134:cerebrospinal fluid*; D006801:Humans; D007375:Interleukin-1 / Q000134:cerebrospinal fluid*; D009414:Nerve Growth Factors / Q000134:cerebrospinal fluid*; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000134:cerebrospinal fluid*; D014409:Tumor Necrosis Factor-alpha / Q000134:cerebrospinal fluid*
D015415:Biomarkers; D007375:Interleukin-1; D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein