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The incidence of Alzheimer's disease (AD) is rising, further increasing the social and economic burden
.
In the absence of any therapeutic intervention, preventive strategies for modifiable risk factors are a promising approach
In observational studies, a new method of using genetic variation to estimate the causal effects of risk factors is Mendelian randomization (MR)
.
Due to the random allocation of genes at conception, MR overcomes the core shortcomings of observational research and assesses the lifetime exposure of risk factors.
Therefore, it can clarify the underlying causality
Andrews et al.
also found that there was no association between the polygenic risk score (PRS, which prioritizes putative causal risk factor scores) increased by SBP and AD risk
Therefore, there is an urgent need for high-quality studies with larger sample sizes to confirm this problem
.
In addition, the expression and function of drug targets can be affected by variations in or near the genes encoding these targets
Therefore, the effects of drugs can be predicted by the genetic effects of their protein target genes, just as they have been applied to lipid-lowering drugs
.
However, only one previous study used the MR method to study the impact of AHMs on the risk of AD, indicating that reducing SBP through the protein target of AHMs is unlikely to affect the risk of AD
Here, considering that the previous MR analysis produced the opposite result, and now there is a larger database of blood pressure characteristics and AD, the Jin-Tai Yu team at Fudan University conducted a two-sample MR analysis for a comprehensive evaluation.
The causal effect of genetic agents of genetically determined blood pressure and antihypertensive drug classes on AD risk
.
They extracted genetic substitutes from genome-wide association studies of BP traits and antihypertensive variants in genes encoding AHM targets
.
The inverse variance weighting method is used as the main model to calculate the estimated value
Result
.
There is limited evidence that the genetic prediction of SBP/diastolic blood pressure levels based on 400/398 single nucleotide polymorphisms (SNPs) affects the risk of AD respectively (all P>0.
The genetic proxy of CCB [odds (OR)=0.
959, 95% confidence interval (CI)=0.
941-0.
977, P=3.
92×10-6] and the overall use of AHM (OR=0.
961, 95%CI=0.
944-0.
978, P=5.
74×10-6, SNPs=52) is related to the low risk of AD
.
No obvious heterogeneity and directional polymorphism were found (all P>0.
05)
.
Other analyses partially support these results
.
None of the SNPs is driving the observed effects
.
The MR analysis found evidence that genetically determined lowering of blood pressure is associated with a lower risk of AD , and CCB has been identified as a promising strategy to prevent AD
.
Original source:
Ou YN, Yang YX, Shen XN, et al.
Genetically determined blood pressure, antihypertensive medications, and risk of Alzheimer's disease: a Mendelian randomization study.
Alz Res Therapy.
2021;13(1):41.
doi:10.
1186 /s13195-021-00782-y
