Premium
P2‐150: Seizures in families with Alzheimer's disease
Author(s) -
Nervi Angela,
Reitz Christiane,
Guillén Maria,
Tang MingXin,
Santana Vincent,
Piriz Angel,
Reyes Dolly,
Lantigua Rafael,
Medrano Martin,
JimenezVelazquez Ivonne,
Lee Joseph,
Mayeux Richard
Publication year - 2011
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2011.05.1036
Subject(s) - dementia , early onset alzheimer's disease , parkinsonism , age of onset , pediatrics , family history , medicine , alzheimer's disease , disease , epilepsy , cohort , psychology , psychiatry
tively normal subjects, 260 with cognitive impairment but no dementia (CIND), and 38 with AD. Serum was assayed in custom multiplexed enzyme-linked immunosorbent assays using high affinity capture antibodies. Each sample was tested in triplicate. Covariates in logistic regression models included age, gender, and education. Results: Among the cognitively normal subjects presence of the APOE e4 allele was associated with elevated serum IL-15 (p 1⁄4 0.025). AD subjects compared to cognitively normal subjects had a higher median serum IL-15 (4.7 vs. 3.6 pg/L; p 1⁄4 0.011). In logistic regression models that included age, education and gender elevated IL-15 was associated with a 2.75-fold increase in AD risk (odds ratio 1⁄4 2.75, 95% confidence interval 1⁄4 1.17, 6.46). Conclusions: The association of elevated IL-15 with the APOE e4 allele in cognitively normal subjects suggests that the APOE e4 allele may increase the risk of AD in part via inflammatory mechanisms. The etiologic importance of the IL-15 association with prevalent cases of AD is uncertain as this could be a cause or consequence of AD pathology or both. Further longitudinal analyses are needed to explore the role of APOE genotype and cytokine biomarkers of inflammation in cognitive decline and the incidence of AD. This work will be important as it might lead to interventions that could reduce neuroinflammatory processes involved in the development of AD.