Scholarlink

Background <p>We investigated the associations of genetic risk score for Alzheimer’s disease (GRS-AD) with cardiometabolic risk from early childhood over a 20-year follow-up.</p> Methods <p>The STRIP study included 1062 children at baseline. GRS-AD was calculated for 631 participants using 22 independent genetic risk variants, including APOE ε2 and ε4 alleles, and excluding them (non-APOE-GRS-AD). We repeatedly measured waist circumference, high-density (HDL-C) and low-density (LDL-C) lipoprotein cholesterol, triglycerides, glucose, insulin, and blood pressure. The data were analysed with generalised additive mixed models.</p> Results <p>GRS-AD was directly associated with serum LDL-C (unstandardised <i>β</i> = 0.140, 95% CI = 0.084 to 0.195) and inversely with HDL-C (<i>β</i> = −0.026, 95% CI = −0.044 to −0.009). GRS-AD was inversely associated with serum HDL-C in males (<i>β</i> = −0.044, 95% CI = −0.070 to −0.018) but not in females (<i>β</i> = −0.010, 95% CI = −0.032 to 0.012). The associations were diluted when the non-APOE-GRS-AD was applied.</p> Conclusion <p>A genetic predisposition to AD may alter lipid metabolism from early childhood.</p> Impact <p><UnorderedList Mark="Bullet"> <ItemContent> <p>While Alzheimer’s disease and cardiometabolic diseases may have shared genetic determinants, the associations between genetic susceptibility for Alzheimer’s disease and increased cardiometabolic risk from childhood to young adulthood are poorly understood.</p> </ItemContent> <ItemContent> <p>We investigated the associations of genetic risk score for Alzheimer’s disease with cardiometabolic risk from early childhood over a 20-year follow-up.</p> </ItemContent> <ItemContent> <p>We found that a higher genetic risk score for Alzheimer’s disease was associated with higher LDL cholesterol, non-HDL cholesterol, and ApoB, and with lower serum HDL cholesterol and ApoA1.</p> </ItemContent> <ItemContent> <p>These findings suggest that a genetic predisposition to Alzheimer’s disease may alter lipid metabolism from early childhood.</p> </ItemContent> </UnorderedList></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Genetic susceptibility to Alzheimer’s disease and cardiometabolic risk from childhood

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月5日

查看全文
  • Eero A. Haapala,
  • Saara Heinonen,
  • Juha Mykkänen,
  • Harri Niinikoski,
  • Hanna Lagström,
  • Pia Salo,
  • Antti Jula,
  • Tapani Rönnemaa,
  • Jorma SA Viikari,
  • Olli T. Raitakari,
  • Katja Pahkala,
  • Suvi Rovio

摘要

Background

We investigated the associations of genetic risk score for Alzheimer’s disease (GRS-AD) with cardiometabolic risk from early childhood over a 20-year follow-up.

Methods

The STRIP study included 1062 children at baseline. GRS-AD was calculated for 631 participants using 22 independent genetic risk variants, including APOE ε2 and ε4 alleles, and excluding them (non-APOE-GRS-AD). We repeatedly measured waist circumference, high-density (HDL-C) and low-density (LDL-C) lipoprotein cholesterol, triglycerides, glucose, insulin, and blood pressure. The data were analysed with generalised additive mixed models.

Results

GRS-AD was directly associated with serum LDL-C (unstandardised β = 0.140, 95% CI = 0.084 to 0.195) and inversely with HDL-C (β = −0.026, 95% CI = −0.044 to −0.009). GRS-AD was inversely associated with serum HDL-C in males (β = −0.044, 95% CI = −0.070 to −0.018) but not in females (β = −0.010, 95% CI = −0.032 to 0.012). The associations were diluted when the non-APOE-GRS-AD was applied.

Conclusion

A genetic predisposition to AD may alter lipid metabolism from early childhood.

Impact

While Alzheimer’s disease and cardiometabolic diseases may have shared genetic determinants, the associations between genetic susceptibility for Alzheimer’s disease and increased cardiometabolic risk from childhood to young adulthood are poorly understood.

We investigated the associations of genetic risk score for Alzheimer’s disease with cardiometabolic risk from early childhood over a 20-year follow-up.

We found that a higher genetic risk score for Alzheimer’s disease was associated with higher LDL cholesterol, non-HDL cholesterol, and ApoB, and with lower serum HDL cholesterol and ApoA1.

These findings suggest that a genetic predisposition to Alzheimer’s disease may alter lipid metabolism from early childhood.