TY - JOUR
T1 - Inflammation in the Alzheimer's disease cascade
T2 - Culprit or innocent bystander?
AU - Tan, Zaldy S.
AU - Seshadri, Sudha
N1 - Funding Information:
This work was supported by the Framingham Heart Study’s National Heart, Lung and Blood Institute contract (N01-HC-25195) and by grants from the National Institute on Aging (R01 AG16495, AG 033040, AG08122, R01 AG033193, P30AG013846 and AG031287). The content is solely the responsibility of the authors and does not necessarily represent the off icial views of the National Institute of Neurological Disorders and Stroke; the National Heart, Lung and Blood Institute; the National Institute on Aging; or the National Institutes of Health.
PY - 2010
Y1 - 2010
N2 - The strongest known risk factors for late-onset Alzheimer disease (LOAD) remain a positive family history and the APOE ε4 allele. van Exel and colleagues used these known risk factors to identify high- and low-risk samples of middle-aged persons in whom they compared levels of inflammatory and vascular risk factors. They observed that, compared with controls, middle-aged offspring of families with a parental history of LOAD had higher blood pressures, lower ankle-brachial indices (measure of peripheral atherosclerosis), and increased production of proinflammatory cytokines in lipopolysaccharide-stimulated whole blood samples, associations that were independent of APOE genotype. This study adds to the growing body of evidence linking inflammatory mechanisms to Alzheimer disease risk and, especially when considered in light of the recently described association of genetic variation in the complement receptor 1 (CR1) gene with LOAD, suggests that inflammatory biomarkers (whether causal or incidental) could be measured and perhaps used to risk-stratify middle-aged persons for early preventive and therapeutic interventions.
AB - The strongest known risk factors for late-onset Alzheimer disease (LOAD) remain a positive family history and the APOE ε4 allele. van Exel and colleagues used these known risk factors to identify high- and low-risk samples of middle-aged persons in whom they compared levels of inflammatory and vascular risk factors. They observed that, compared with controls, middle-aged offspring of families with a parental history of LOAD had higher blood pressures, lower ankle-brachial indices (measure of peripheral atherosclerosis), and increased production of proinflammatory cytokines in lipopolysaccharide-stimulated whole blood samples, associations that were independent of APOE genotype. This study adds to the growing body of evidence linking inflammatory mechanisms to Alzheimer disease risk and, especially when considered in light of the recently described association of genetic variation in the complement receptor 1 (CR1) gene with LOAD, suggests that inflammatory biomarkers (whether causal or incidental) could be measured and perhaps used to risk-stratify middle-aged persons for early preventive and therapeutic interventions.
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U2 - 10.1186/alzrt29
DO - 10.1186/alzrt29
M3 - Comment/debate
C2 - 20388190
AN - SCOPUS:77953827925
SN - 1758-9193
VL - 2
JO - Alzheimer's Research and Therapy
JF - Alzheimer's Research and Therapy
IS - 1
M1 - 6
ER -