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Prenatal exposure to the pesticide DDT metabolite DDE was linked to lower levels of a key Alzheimer's biomarker and poorer cognitive function in midlife. This suggests DDT/DDE exposure may increase Alzheimer's and Related Dementias (ADRD) risk.

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Area of Science:

  • Environmental Health
  • Neuroscience
  • Toxicology

Background:

  • Environmental exposures are increasingly recognized as risk factors for Alzheimer's and Related Dementias (ADRD).
  • Previous research linked higher serum DDE (a persistent DDT metabolite) to increased Alzheimer's risk and cognitive decline.
  • Animal studies show DDT/DDE reduce cognitive function and increase amyloid pathology, indicated by lower plasma Aβ 42/40 ratio.

Purpose of the Study:

  • To investigate the effects of prenatal DDE exposure on plasma amyloid-beta (Aβ) levels and cognitive function in humans.
  • To assess the association between prenatal DDE exposure and midlife cognitive performance and Aβ 42/40 ratio.

Main Methods:

  • Utilized data from the Child Health and Development Studies (CHDS) pregnancy cohort (1959-1963).
  • Assessed midlife cognitive function using the Digit Symbol Test (DSST) and measured plasma Aβ 42/40 ratio in 179 participants.
  • Measured prenatal p,p'-DDE levels in archived maternal serum and analyzed associations using generalized linear regression models.

Main Results:

  • Prenatal p,p'-DDE levels were significantly associated with lower midlife plasma Aβ 42/40 ratio (β = -0.37, p = 0.03).
  • Higher prenatal p,p'-DDE levels correlated with worse performance on the DSST in midlife (β = -0.020, p = 0.02).
  • These associations remained robust after adjusting for covariates.

Conclusions:

  • Prenatal exposure to p,p'-DDE is associated with altered Aβ 42/40 levels and impaired cognitive function in midlife.
  • Identifying populations with higher DDT/DDE exposure may help pinpoint individuals at increased risk for ADRD.
  • Early intervention and prevention strategies can be developed for those at risk of ADRD progression.