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311.
  • Iacono, Diego, et al. (författare)
  • Neuropathologic Assessment of Dementia Markers in Identical and Fraternal Twins
  • 2014
  • Ingår i: Brain Pathology. - 1015-6305 .- 1750-3639. ; 24:4, s. 317-333
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Twin studies are an incomparable source of investigation to shed light on genetic and non-genetic components of neurodegenerative diseases, as Alzheimer's disease (AD). Detailed clinicopathologic correlations using twin longitudinal data and post-mortem examinations are mostly missing. We describe clinical and pathologic findings of seven monozygotic (MZ) and dizygotic (DZ) twin pairs. Our findings show good agreement between clinical and pathologic diagnoses in the majority of the twin pairs, with greater neuropathologic concordance in MZ than DZ twins. Greater neuropathologic concordance was found for -amyloid than tau pathology within the pairs. ApoE4 was associated with higher -amyloid and earlier dementia onset, and importantly, higher frequency of other co-occurring brain pathologies, regardless of the zygosity. Dementia onset, dementia duration, difference between twins in age at dementia onset and at death, did not correlate with AD pathology. These clinicopathologic correlations of older identical and fraternal twins support the relevance of genetic factors in AD, but not their sufficiency to determine the pathology, and consequently the disease, even in monozygotic twins. It is the interaction among genetic and non-genetic risks which plays a major role in influencing, or probably determining, the degeneration of those brain circuits associated with pathology and cognitive deficits in AD.</p>
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312.
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316.
  • Karlsson, Ida K., et al. (författare)
  • Apolipoprotein E DNA methylation and late-life disease
  • 2018
  • Ingår i: International Journal of Epidemiology. - Oxford University Press. - 0300-5771 .- 1464-3685. ; 47:3, s. 899-907
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>Background:</strong> This study aims to investigate if DNA methylation of the apolipoprotein E (APOE) locus affects the risks of dementia, Alzheimers disease (AD) or cardiovascular disease (CVD).</p><p><strong>Methods:</strong> DNA methylation across the APOE gene has previously been categorized into three distinct regions: a hypermethylated region in the promoter, a hypomethylated region in the first two introns and exons and a hypermethylated region in the 3'exon that also harbours the APOE epsilon 2 and epsilon 4 alleles. DNA methylation levels in leukocytes were measured using the Illumina 450K array in 447 Swedish twins (mean age 78.1 years). We used logistic regression to investigate whether methylation levels in those regions affect the odds of disease.</p><p><strong>Results:</strong> We found that methylation levels in the promoter region were associated with dementia and AD after adjusting for sex, age at blood draw, education, smoking and relatedness among twins [odds ratio (OR) 1.32 per standard deviation increase in methylation levels, 95% confidence interval (CI) 1.08-1.62 for dementia; OR 1.38, 95% CI 1.07-1.78 for AD). We did not detect any difference in methylation levels between CVD cases and controls. Results were similar when comparing within discordant twin pairs, and did not differ as a function of APOE genotype.</p><p><strong>Conclusions:</strong> We found that higher DNA methylation levels in the promoter region of APOE increase the odds of dementia and AD, but not CVD. The effect was independent of APOE genotype, indicating that allelic variation and methylation variation in APOE may act independently to increase the risk of dementia.</p>
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317.
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320.
  • Karlsson, Ida K., et al. (författare)
  • Genetic influences on body mass index across Adulthood and late-life
  • 2018
  • Ingår i: Innovation in Aging. - Oxford University Press. - 1556-343X. ; 2:suppl_1, s. 620-620
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Although genetic factors significantly contribute to variation in body-mass index (BMI), the effects appear to differ with age. To investigate this, we applied polygenic methods to longitudinal data from the Swedish Twin Registry where BMI was available for age categories ranging from 20–35 to above 80. Using GCTA, a polygenic method to estimate heritability, we showed that heritability explains around 20% of the variability in BMI across age categories. However, a polygenic risk score based on the largest GWAS of BMI (PRSBMI) explained 4–6% of the variation in BMI before 65, but less than 0.5% after age 65. This indicates that while there is substantial heritability of BMI across adulthood and late-life, the genetic variants identified in GWAS mainly predict BMI before age 65. Hence, more work is warranted studying the genetics of BMI in late-life, to better understand its biology and what distinguishes it from BMI earlier in adulthood.</p>
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