Several strengths, lacks details
, professor of epidemiology and director of the National Alzheimer’s Coordinating Center at the University of Washington, Seattle, noted that the investigators appear to have implemented their chosen methods of causal association analysis well. “They attempted to examine the direction of the causal arrow for risk factors … and that is a step usually not well examined in other studies.”
He added that the collection of objective measures, such as of sleep, is another strength of the study.
However, “the common weakness of the basic GWAS sample is that clinical symptomatology determined Alzheimer’s disease diagnosis. Thus, asymptomatic or very mildly symptomatic persons with Alzheimer’s disease pathology in their brains were likely included among normal controls,” said Dr. Kukull, who was not involved with the research.
Because of an apparent lack of biomarker data, patients who had been diagnosed with Alzheimer’s disease may in fact have had a different form of dementia. Given the nature of their data, the investigators could have done little to compensate for these possibilities, Dr. Kukull added. In addition, the article lacks details that would improve the interpretation of the results.
“Timing is everything with regard to potential associations between risk factor and outcome,” Dr. Kukull said. “With the exceptions of genes, it would be nice to know more about the timing of risk factors’ onset and Alzheimer’s disease onset.”
Still, the results indicate potential areas of future study, he noted. “Primarily, further research must address the question of pathological onset of disease and misclassification of diagnosis in both cases and controls due to lack of biomarker-confirmed diagnosis. Then research can also struggle with the timing of potential risk factors with respect to disease.”
The study was funded by the U.K. Dementia Research Institute. Dr. Dehghan and Dr. Kukull reported no relevant financial relationships.
A version of this article originally appeared on.