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Basic Science and Pathogenesis.

Junkai Xie1, Shichen Wu1, Han Zhao1

  • 1Purdue University, West Lafayette, IN, USA.

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Lead (Pb) exposure during development and adulthood can trigger Alzheimer's disease (AD) hallmarks like tau tangles and amyloid plaques. This study reveals Pb exposure causes neuronal dysfunction and heightened AD susceptibility, even after exposure ceases.

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Area of Science:

  • Neuroscience
  • Toxicology
  • Genomics

Background:

  • Environmental lead (Pb) exposure is linked to neurological deficits and Alzheimer's disease (AD) risk.
  • Epidemiological and animal studies support a connection, but molecular mechanisms are unclear.

Purpose of the Study:

  • Investigate Pb exposure's impact on Alzheimer's disease (AD)-like pathogenesis in human neurons.
  • Examine effects across different life stages and at environmentally relevant Pb concentrations.

Main Methods:

  • Used human induced pluripotent stem cell (hiPSC)-derived cortical neurons.
  • Assessed neurological effects using immunofluorescence, Western blotting, RNA sequencing, ELISA, and microelectrode array (MEA).
  • Employed a "secondary hit" model with relevant stressors like PHF-Tau and MPP+.

Main Results:

  • Pb exposure caused neuronal hyperactivity and mitochondrial dysfunction.
  • Transcriptomic analysis revealed altered oxidative phosphorylation and AD-related pathways.
  • Observed increased phosphorylated Tau, Tau aggregates, and Aβ42/40 ratios, hallmarks of AD.
  • Pb-exposed neurons showed persistent increased susceptibility to secondary stressors.

Conclusions:

  • Pb exposure contributes to AD pathogenesis via specific molecular pathways.
  • Findings elucidate mechanisms linking environmental Pb exposure to increased AD risk.