Lymphocyte mitochondria: toward identification of peripheral biomarkers in the progression of Alzheimer disease
Open accessAbstract
Alzheimer disease (AD) is an age-related neurodegenerative condition. AD is histopathologically characterized by the presence of three main hallmarks: senile plaques (rich in amyloid-β peptide), neuronal fibrillary tangles (rich in phosphorylated tau protein), and synapse loss. However, definitive biomarkers for this devastating disease in living people are still lacking. In this study, we show that levels of oxidative stress markers are significantly increased in the mitochondria isolated from lymphocytes of subjects with mild cognitive impairment (MCI) compared to cognitively normal individuals. Further, an increase in mitochondrial oxidative stress in MCI is associated with MMSE score, vitamin E components, and β-carotene. Further, a proteomics approach showed that alterations in the levels of thioredoxin-dependent peroxide reductase, myosin light polypeptide 6, and ATP synthase subunit β might be important in the progression and pathogenesis of AD. Increased understanding of oxidative stress and protein alterations in easily obtainable peripheral tissues will be helpful in developing biomarkers to combat this devastating disorder.
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In people with aMCI or AD, mitochondria from peripheral lymphocytes show elevated oxidative stress.
“Using a different approach, oxidative stress was found to be elevated in mitochondria isolated from peripheral lymphocytes of people with aMCI and AD76”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [76]
The Results (Oxidative stress markers; page unavailable) report significantly increased oxidation markers in mitochondria from MCI lymphocytes. The Discussion (page unavailable) also reports increased oxidative-stress markers in AD lymphocyte mitochondria, citing the authors’ earlier work. Our copy identifies the studied group as MCI, not specifically amnestic MCI (aMCI), so it does not establish that qualifier. (LLM, conf=0.84)
Experimental — accuracy not yet measuredRedox proteomics identified similar proteins as identified in AD and MCI brains as oxidatively modified, including mitochondrial ATP synthase.
“Redox proteomics identified similar proteins as identified in AD and MCI brains as oxidatively modified, and these included mitochondrial ATP synthase [36,37].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [37]
The Results (Alterations of protein levels in mitochondria; page unavailable) identify ATP synthase subunit beta among proteins with altered levels in lymphocyte mitochondria. The Discussion (page unavailable) says these proteins had also been reported as altered in AD and MCI brain, but it does not show that ATP synthase was identified as oxidatively modified by redox proteomics. (LLM, conf=0.88)
Experimental — accuracy not yet measuredLevels of protein-bound carbonyls, 3-NT, and HNE are significantly increased in mitochondria isolated from lymphocytes of MCI and AD patients, and these correlate with elevated Aβ levels, decreased levels of small molecule antioxidants, and decreased cognitive test performance.
“Levels of protein-bound carbonyls, 3-NT, and HNE are significantly increased in mitochondria isolated from lymphocytes of MCI and AD patients, which correlate with elevated Aβ levels, decreased levels of small molecule antioxidants, and decreased cognitive test performance [36,37].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [37]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredMitochondria isolated from lymphocytes from persons with AD and MCI show elevated oxidative damage that correlates inversely with cognitive performance.
“mitochondria isolated from lymphocytes from persons with AD and MCI showed elevated oxidative damage that correlated inversely with cognitive performance [36,37].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [37]
Significant increases in all the proteins affected in MCI lymphocyte mitochondria were detected.
“Interestingly, significant increases in all the proteins affected in MCI lymphocyte mitochondria were detected.”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [37]
The proteins with altered expression in MCI and AD lymphocyte mitochondria can be categorized as involved in energetics, structural integrity, cell signaling, and antioxidant defense.
“These proteins can be categorized as involved in energetics, structural integrity, cell signaling, and antioxidant defense [37].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [37]
Quantitative proteomics identified protein expression alterations in mitochondria isolated from both MCI and AD lymphocytes.
“Further study using quantitative proteomics identified protein expression alterations in mitochondria isolated from both MCI and AD lymphocytes.”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [37]
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- Authors
- Sultana, R., Baglioni, M., Cecchetti, R., Cai, J., Klein, J. B., Bastiani, P., Ruggiero, C., Mecocci, P., & Butterfield, D. A.
- Affiliations
- University of Perugia (IT)
- University of Louisville (US)
- University of Kentucky (US)
- Corresponding author
- Butterfield, D. Allan
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 65
- Pages
- 595-606
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC3849349
- OpenAlex
- W1996129582
- Cited by
- 64
- References
- 67
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 4 · 2023: 3 · 2022: 5 · 2021: 5 · 2020: 6 · 2019: 3 · 2018: 8 · 2017: 4 · 2016: 5 · 2015: 7 · 2014: 11 · 2013: 1
- FWCI
- 5.57
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (AG-05119)
- Italian Ministry of Research (PRIN 20078TC4E5)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- Alzheimer's disease, mild cognitive impairment, oxidative stress, peripheral biomarkers, mitochondrial proteomics, ATP synthase beta subunit, vitamin E, beta-carotene, disease progression
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Female, Humans, Isoelectric Focusing, Lymphocytes, Male, Mitochondria, Mass Spectrometry, Electrophoresis, Gel, Two-Dimensional, Biomarkers, Oxidative Stress, Disease Progression, Proteomics, Cognitive Dysfunction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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