A study published in the latest edition of the journal PLOS Medicine used gene variant analysis to assess the association between modifiable risk factors and individual patient susceptibility to being diagnosed with Alzheimer’s Disease (AD). The study, entitled “Associations between Potentially Modifiable Risk Factors and Alzheimer Disease: A Mendelian Randomization Study” was led by Robert Scott of the MRC Epidemiology Unit at University of Cambridge in collaboration with teams of researchers across the globe.
The international collaborative team of investigators utilized a standardized method of genetic analysis, in which they distinguished gene variants in a large number of single nucleotide polymorphisms (SNPs). SNPs are the most common cause of genetic variation in organisms. These differences are due to a change in a nucleotide, which is the building block of DNA. Researchers use SNPs to help identify susceptibility factors to diseases such as AD.
Numerous studies have established that there are several potential risk factors for AD, but the causative influence of these factors on diagnosis is still not understood. Without knowledge of a causative agent, it is unclear whether certain interventions to modify risk behaviors will have any benefit in preventing an individual’s diagnosis of AD.
In an effort to understand the causative nature of these risk factors on AD diagnosis the researchers analyzed SNPs in genetic data from 17,008 individuals with AD and 37,154 cognitively normal elderly controls collected by the International Genomics of Alzheimer’s Project. They compared both groups by modifiable risk factors including blood pressure (BP), smoking, cholesterol levels, Body Mass Index (BMI), and educational levels.
The primary study finding showed that genetic variants that predict higher systolic blood pressure (the pressure exerted on the inside of large blood vessels when the heart is pumping out blood) are associated with a higher probability of taking antihypertensive (lower BP) medication and with decreased risk of AD. Other important analytic observations were that certain predicted smoking quantities was also associated with lower AD risk, but there was no evidence of causal associations between any of the other risk factors investigated and AD risk.
When discussing the findings, the authors wrote, “since there is a strong association between higher SBP gene scores and exposure to antihypertensive treatments, there is a need to evaluate the possible protective role of some of these substances against AD, independent of their effects on blood pressure.”
Further confirmatory studies need to be conducted to understand this “possible protective role.”
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