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Basic Science and Pathogenesis.

Thi Kim Oanh Nguyen1, Sergey A Trushin1, Mark Ostroot1

  • 1Department of Neurology, Mayo Clinic, Rochester, MN, USA.

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|December 24, 2025
PubMed
Summary
This summary is machine-generated.

Mild inhibition of mitochondrial complex I (mtCI) with CP2 enhances glucose metabolism and brain energy homeostasis, offering a potential new therapeutic strategy for Alzheimer's disease (AD). This approach shows promise for delaying AD onset and progression.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Alzheimer's disease (AD) necessitates novel treatments beyond amyloid-beta (Aβ) targeting.
  • Mitochondrial dysfunction and impaired brain energy homeostasis are early AD hallmarks.
  • Mitochondrial complex I (mtCI) inhibition is a potential therapeutic strategy.

Purpose of the Study:

  • To elucidate the mechanistic link between mtCI inhibition, glucose metabolism, and energy homeostasis in AD.
  • To assess the impact of mtCI inhibition on cellular energy metabolism in AD models.

Main Methods:

  • Assessed cellular energy metabolism in APPswe-expressing neuroblastoma cells and controls using Seahorse Analyzer.
  • Measured glycolytic function, mitochondrial energetics, fatty acid β-oxidation (FAO), and glucose uptake.
  • Analyzed GLUT translocation, protein expression, and specific metabolites via flow cytometry, Western blot, and mass spectrometry.

Main Results:

  • APPswe cells showed reduced glycolysis and respiratory capacity, with partial compensation by FAO.
  • CP2 treatment acutely enhanced glucose transporter (GLUT) translocation and glucose uptake.
  • CP2 facilitated glucose utilization in oxidative phosphorylation (OXPHOS) via AMPK, enhancing TCA cycle function.

Conclusions:

  • Mild mtCI inhibition activates neuroprotective mechanisms, including improved glucose metabolism and energy homeostasis.
  • CP2 demonstrates therapeutic potential for Alzheimer's disease by addressing energy deficits.
  • Findings in human cells and AD mouse models support the translational viability of this approach.