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Basic Science and Pathogenesis.

Evelyn Pardo1, Vijay Kumar Sagar1, Kelly Kim1

  • 1University of Virginia, Charlottesville, VA, USA.

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|December 23, 2025
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Summary
This summary is machine-generated.

Nutrient-induced Mitochondrial Activity (NiMA) disruption occurs early in Alzheimer's disease (AD) pathogenesis. Amyloid-beta oligomers and APOE4 expression disrupt NiMA, impacting mitochondrial function before AD symptoms appear.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is characterized by mitochondrial dysfunction, oxidative stress, and mTOR dysregulation.
  • Nutrient-induced Mitochondrial Activity (NiMA) is an inter-organelle signaling pathway linking insulin, lysosomal mTORC1, and mitochondrial function in neurons.
  • Amyloid-beta oligomers (AβOs) were previously shown to downregulate NiMA via mTORC1 activation and SOD1 upregulation.

Purpose of the Study:

  • To investigate if AβOs and APOE4 disrupt NiMA at presymptomatic stages of AD.
  • To elucidate the molecular mechanisms underlying NiMA disruption in early AD.

Main Methods:

  • Utilized two-photon fluorescence lifetime imaging to record live mitochondrial metabolism in APP knock-in (APPKI) and APOE4 knock-in (APOE4KI) mice.
  • Employed GSK3β inhibition and BioID proximity labeling to explore molecular mechanisms.

Main Results:

  • NiMA was downregulated in 4-month-old APPKI mice and completely blocked by 6 months, preceding AD pathology.
  • GSK3β signaling through mTORC1 regulates SOD1 and mitochondrial activity; GSK3β inhibition partially restored mitochondrial function.
  • NiMA was downregulated in 2-month-old APOE4KI mice, representing the earliest molecular dysfunction linked to APOE4.
  • Identified 10 potential novel regulators of NiMA using BioID.

Conclusions:

  • NiMA disruption is an early, fundamental event in Alzheimer's disease pathogenesis.
  • This pathway connects nutrient sensing, mTORC1 activity, and cellular redox to neuronal mitochondrial function.