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Proton pump inhibitors: predisposers to Alzheimer disease?

M K Fallahzadeh1, A Borhani Haghighi, M R Namazi

  • 1Autoimmune Diseases Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

Journal of Clinical Pharmacy and Therapeutics
|May 12, 2010
PubMed

Insights

Proton pump inhibitors (PPIs) may hinder the brain

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Alzheimer disease (AD) pathogenesis involves abnormal amyloid-beta peptide (A beta) processing and fibrillar A beta (fA beta) formation.
  • Microglia, the brain's immune cells, clear fA beta via acidic lysosomes, but lysosomal acidity is reduced in AD patients.
  • Vacuolar proton pumps (V-ATPases) acidify lysosomes; proton pump inhibitors (PPIs) block these pumps.

Purpose of the Study:

  • To investigate the potential impact of proton pump inhibitors (PPIs) on microglial lysosomal function and amyloid-beta clearance.
  • To explore the hypothesis that PPIs may represent a risk factor for Alzheimer disease development or progression.

Main Methods:

  • The study focuses on the mechanism of V-ATPases in microglial lysosomes and the effect of PPIs on lysosomal pH.
  • It considers the known penetration of PPIs across the blood-brain barrier and their widespread, long-term use.

Main Results:

  • PPIs' inhibition of V-ATPases could lead to lysosomal basification in microglia.
  • This reduced acidity may impair the degradation of fibrillar amyloid-beta (fA beta).

Conclusions:

  • Chronic consumption of proton pump inhibitors may compromise microglial amyloid-beta clearance.
  • This mechanism suggests that long-term PPI use could be a potential risk factor for Alzheimer disease.

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