Current knowledge about the pathogenic mechanism of Alzheimer's disease is based mainly on rare, high-penetrance variants in genes encoding amyloid precursor protein, presenilin 1, and presenilin 2, which result in familial early-onset Alzheimer's disease. However, Alzheimer's disease is predominantly a sporadic late-onset disease with exponentially increasing prevalence starting at the age of 65 years. Genomewide association studies have recently identified several risk variants for late-onset Alzheimer's disease, but aside from the well-known ε4 allele of apolipoprotein E, these variants are generally associated with very low risk; in addition, such variants are noncoding and more challenging to link to molecular function. . . .
CITATION STYLE
Neumann, H., & Daly, M. J. (2013). Variant TREM2 as Risk Factor for Alzheimer’s Disease. New England Journal of Medicine, 368(2), 182–184. https://doi.org/10.1056/nejme1213157
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