Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.neurobiolaging.2017.11.012
Title: Case-control analysis of leucine-rich repeat kinase 2 protective variants in Alzheimer's disease
Authors: Ng A.S.L. 
Ng E.Y.L.
Tan Y.J. 
Kandiah N. 
Zhou J. 
Hameed S. 
Ting S.K.S. 
Tan E.-K. 
Keywords: Alzheimer's disease
Genes
LRRK2
Variants
Issue Date: 2018
Publisher: Elsevier Inc.
Citation: Ng A.S.L., Ng E.Y.L., Tan Y.J., Kandiah N., Zhou J., Hameed S., Ting S.K.S., Tan E.-K. (2018). Case-control analysis of leucine-rich repeat kinase 2 protective variants in Alzheimer's disease. Neurobiology of Aging 64 : 157.e7-157.e9. ScholarBank@NUS Repository. https://doi.org/10.1016/j.neurobiolaging.2017.11.012
Abstract: Amyloid is the main pathological substrate of Alzheimer's disease (AD) and has been described in leucine-rich repeat kinase 2 (LRRK2) carriers with Parkinson's disease. LRRK2 has been linked with amyloid precursor protein pathways in neurodegeneration. Two common LRRK2 variants, R1398H and N551K, have been shown to be protective in multiple Parkinson's disease cohorts. We hypothesized that R1398H and N551K may be protective in AD. In a case-control study involving 1390 subjects (719 controls and 671 AD cases), R1398H was demonstrated in 16.8% of AD cases compared to 16.7% in controls (odds ratio = 1.01, 95% confidence interval = 0.76�1.34, p = 0.94), whereas N551K was demonstrated in 17.3% of AD cases compared to 17.2% of controls (odds ratio = 1.00, 95% confidence interval = 0.76�1.32, p = 0.98). Overall, these results suggest that LRRK2 R1398H or N551K variants do not appear to modulate the risk of AD. � 2017 Elsevier Inc.
Source Title: Neurobiology of Aging
URI: http://scholarbank.nus.edu.sg/handle/10635/148930
ISSN: 01974580
DOI: 10.1016/j.neurobiolaging.2017.11.012
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