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Chronic exposure to cadmium (Cd) and lead (Pb) worsens cognitive decline and Alzheimer

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Area of Science:

  • Neuroscience
  • Toxicology
  • Cellular Biology

Background:

  • Epidemiological studies link heavy metal exposure, like cadmium (Cd) and lead (Pb), to increased Alzheimer's disease (AD) risk.
  • The precise cellular and molecular mechanisms by which Cd and Pb influence AD pathogenesis remain largely unknown.
  • This study investigates the impact of Cd and Pb exposure on cognitive function and AD progression in a 5xFAD mouse model.

Purpose of the Study:

  • To determine how chronic exposure to cadmium (Cd) and lead (Pb) affects cognitive function in the 5xFAD mouse model of Alzheimer's disease (AD).
  • To elucidate the cellular and molecular mechanisms underlying the exacerbation of AD pathogenesis by Cd and Pb exposure.

Main Methods:

  • 5xFAD mice were exposed to lead (Pb) or cadmium (Cd) in drinking water for 6 weeks.
  • Cognitive functions were assessed using Y-maze and Open Field Maze tests.
  • Senescence markers, senescence-associated secretory phenotype (SASP) cytokines, and neuroinflammation markers were analyzed using RT-PCR, immunofluorescence, and confocal microscopy.

Main Results:

  • Both Cd and Pb exposure accelerated amyloid-beta (Aβ) plaque formation and cognitive decline in 5xFAD mice.
  • Cd exposure, even at a lower dose, was more potent than Pb in exacerbating Aβ deposition and cognitive deficits.
  • Cd exposure increased p16Ink4a senescence marker and IL-6 expression, particularly in the hippocampus, and induced premature senescence in microglial cells.

Conclusions:

  • Chronic exposure to Cd or Pb exacerbates cognitive deficits and Alzheimer's disease (AD) progression in 5xFAD mice.
  • Cd exposure accelerates AD progression by increasing senescent cell burden and neuroinflammation in the hippocampus.
  • Senescent microglia, induced by Cd, contribute to neuroinflammation via IL-6 release.