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Basic Science and Pathogenesis.

Josephine Chu1, Ross A Steinberg1, Brian Carson1

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Alcohol-induced liver injury exacerbates Alzheimer's Disease (AD) by increasing amyloid precursor protein (APP) in liver mitochondria. This suggests liver mitochondria may produce peripheral amyloid beta (aB), contributing to AD progression.

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Area of Science:

  • Hepatology
  • Neuroscience
  • Mitochondrial Biology

Background:

  • Alcohol-induced liver injury impacts the pericentral liver region, affecting mitochondrial function and potentially worsening Alzheimer's Disease (AD) progression.
  • Mitochondrial subpopulations (GM, PDM, ERM) are crucial for cellular homeostasis, energy production, and calcium regulation.
  • Hepatic amyloid precursor protein (APP) is linked to peripheral amyloid beta (aB) production and AD pathology.

Purpose of the Study:

  • To investigate the site-specific expression and localization of hepatic APP and aB processing proteins within mitochondrial subpopulations in ethanol-fed AD mice.
  • To understand the role of hepatic mitochondria in aB metabolism and its potential contribution to AD pathogenesis.

Main Methods:

  • Utilized double transgenic (APP/PS1) AD mice fed ethanol or control diets for 5 weeks.
  • Employed digital spatial profiling (DSP) to analyze AD biomarkers (APP, PSEN1, BACE1) in liver tissue.
  • Isolated mitochondrial fractions via differential centrifugation for western blotting analysis.

Main Results:

  • Mitochondrial APP and PSEN1 expression significantly increased compared to the cytosol in AD mice, irrespective of ethanol feeding.
  • Ethanol feeding led to increased APP expression in general mitochondria (GM) and ER-bound mitochondria (ERM), but not peridroplet mitochondria (PDM).
  • APP transcript levels rose in the pericentral liver region of ethanol-fed mice, with trends for increased APP and aB protein levels.

Conclusions:

  • Differential APP expression across mitochondrial subpopulations indicates hepatic mitochondria as a potential source of peripheral aB.
  • Increased hepatic APP in the pericentral region aligns with alcohol-induced liver damage sites, suggesting a link to AD progression.
  • Further research modulating hepatic APP is needed to elucidate its contribution to AD pathogenesis.