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Basic Science and Pathogenesis.

Leandro Ceotto Freitas Lima1, Kevin P Kotredes2, Juliet A Moncaster3

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Environmental toxicants like lead, cadmium, and arsenic accumulate in the brain and alter gene expression, increasing Alzheimer

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Area of Science:

  • Neuroscience
  • Environmental Health
  • Toxicology

Background:

  • Alzheimer's disease (AD) and AD-related dementias (ADRD) are linked to environmental toxicants, but mechanisms are unclear.
  • Genetic risk variants for AD can synergize with neurotoxic metal (lead, cadmium) and metalloid (arsenic) exposures.
  • These toxicants cross the blood-brain barrier (BBB), disrupt neuronal function, and modulate AD pathways.

Purpose of the Study:

  • To investigate how lead (Pb), cadmium (Cd), and arsenic (As) exposures alter AD-linked gene expression.
  • To determine if these exposures potentiate AD pathogenesis in a toxicant-specific and age-dependent manner.
  • To establish the TOX-AD consortium as an exposome resource for AD/ADRD research.

Main Methods:

  • MODEL-AD mice were exposed to Pb, Cd, or As via drinking water for 30 days.
  • A separate cohort of B6.APPSwDI mice was exposed to Pb to assess BBB integrity.
  • Blood and brain tissues were collected for toxicant level analysis and gene expression profiling.

Main Results:

  • Exposed animals showed increased metal/metalloid levels in blood and brain.
  • Gene expression changes included increased VGF (Pb, As) and decreased APP (Cd).
  • Pb exposure disrupted BBB integrity, increased Aβ ratio, and promoted Aβ deposition, with significant gene ontology associations for Pb, As, and Cd related to AD pathobiology.

Conclusions:

  • Pb, Cd, and As exposure leads to toxicant accumulation in blood and brain.
  • These exposures induce toxicant-specific alterations in gene expression relevant to AD.
  • The findings highlight the role of environmental toxicants in AD pathobiology.