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Lymphocytic mitochondrial aconitase activity is reduced in Alzheimer's disease and mild cognitive impairment

Francesca Mangialasche1, Mauro Baglioni2, Roberta Cecchetti2

  • 1Section of Gerontology and Geriatrics, Department of Medicine, University of Perugia, Perugia, Italy Aging Research Center, Karolinska Institutet-Stockholm University, Stockholm, Sweden.

Journal of Alzheimer'S Disease : JAD
|October 18, 2014
PubMed
Abstract

Insights

Reduced mitochondrial aconitase (ACO2) activity in blood lymphocytes is linked to Alzheimer's disease (AD) and mild cognitive impairment (MCI). Lower ACO2 activity correlates with cognitive decline and antioxidant levels, suggesting its potential as an AD biomarker.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Mitochondrial Biology

Background:

  • Oxidative stress and mitochondrial dysfunction are implicated in Alzheimer's disease (AD) pathogenesis.
  • Mitochondrial aconitase (ACO2), a Krebs cycle enzyme, is sensitive to free radical damage.

Purpose of the Study:

  • To assess ACO2 activity and expression in lymphocytes of AD, mild cognitive impairment (MCI), and cognitively normal individuals.
  • To evaluate the correlation between ACO2 levels, antioxidant status, and cognitive function.

Main Methods:

  • Collected blood samples from AD, MCI, older normal cognition (OCN), and younger normal cognition (YCN) groups.
  • Measured ACO2 activity in lymphocytes, including assessment after in vitro free radical exposure.
  • Quantified plasma antioxidant levels and ACO2 expression.

Main Results:

  • Significantly lower ACO2 activity was observed in AD and MCI groups compared to controls.
  • ACO2 expression was reduced in AD and MCI subjects.
  • ACO2 activity positively correlated with vitamin E levels and cognitive scores (MMSE).
  • AD lymphocytes showed greater ACO2 activity reduction upon free radical exposure.

Conclusions:

  • Reduced ACO2 activity in peripheral lymphocytes may indicate AD and MCI.
  • ACO2 activity correlates with antioxidant protection and cognitive status.
  • ACO2 warrants further investigation as a potential biomarker for AD pathogenesis and progression.
Keywords:
Aconitase (aconitate hydratase)Alzheimer diseaseantioxidantsfree radicalslymphocytemild cognitive impairmentmitochondriaoxidative stressreactive nitrogen speciesreactive oxygen species

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