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Summary
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Midlife exposure to dichlorodiphenyldichloroethylene (DDE) alters fatty acid and amino acid metabolism, mirroring changes linked to cognitive decline and Alzheimer's Disease (AD). These findings suggest potential early biomarkers for AD risk.

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Area of Science:

  • Environmental Health
  • Metabolomics
  • Neurodegenerative Diseases

Background:

  • Serum dichlorodiphenyldichloroethylene (DDE), a metabolite of DDT, is linked to cognitive impairment and Alzheimer's Disease (AD) risk.
  • High-resolution metabolomics reveals metabolic phenotypes associated with early cognitive changes and AD.
  • Metabolic alterations in midlife serum related to DDE preceding cognitive dysfunction require characterization.

Purpose of the Study:

  • To characterize midlife serum metabolome changes associated with dichlorodiphenyldichloroethylene (DDE) exposure.
  • To investigate potential metabolic precursors to cognitive dysfunction and AD.

Main Methods:

  • Analysis of 362 subjects from the Child Health and Development Studies (CHDS) cohort.
  • Cross-sectional analysis of midlife serum p,p'-DDE, metabolome, and exposome using LC-MS and GC-MS.
  • Metabolome-wide association study (MWAS) to identify DDE-associated metabolic pathways.

Main Results:

  • p,p'-DDE was associated with alterations in fatty acid metabolism pathways (carnitine shuttle, biosynthesis, arachidonic acid, prostaglandin, glycerophospholipid).
  • Metabolism of alanine and aspartate amino acids were linked to p,p'-DDE.
  • Decreased levels of essential fatty acids (DHA, EPA) and acylcarnitines were observed with increasing serum p,p'-DDE.

Conclusions:

  • Midlife DDE-associated metabolic changes overlap with those linked to cognitive dysfunction and AD.
  • These findings highlight potential metabolic mediators in cognitive decline and AD onset.
  • Relating midlife serum DDE and metabolome may elucidate biological mechanisms in AD.