Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Quantitative profiling brain proteomes revealed mitochondrial dysfunction in Alzheimer's disease.

Sunil S Adav1,2, Jung Eun Park3, Siu Kwan Sze4

  • 1School of Biological Sciences, Division of Structural Biology and Biochemistry, Nanyang Technological University, 60 Nanyang Drive, Singapore, 637551, Singapore. ssadav@ntu.edu.sg.

Molecular Brain
|January 30, 2019
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Protective Effects of <i>Momordica charantia</i> Extract on Dexamethasone-Induced Sarcopenic Changes in C2C12 Cells: Integrated Network Pharmacology and Experimental Validation.

Pharmaceuticals (Basel, Switzerland)·2026
Same author

An Exploratory Study on Beneficial Effect of BE-FD-1 (Mineral-Enriched <i>Raphanus sativus</i> L. Leaf Extract) in High-Fat-Diet- and Streptozotocin-Induced Diabetic Mice.

Nutrients·2026
Same author

Performance validation of the KeraSkin™ reconstructed human epidermis (RhE) model according to OECD document no. 219 and exploratory optimization of its predictive capacity for in vitro skin corrosion testing.

Toxicology in vitro : an international journal published in association with BIBRA·2026
Same author

PSEN1 mutant marmoset fibroblasts mimic multi-omic signatures of Alzheimer's disease.

bioRxiv : the preprint server for biology·2026
Same author

The evolving landscape of recombinant adeno-associated virus (rAAV) manufacturing: Engineering vector plasmids for upstream production.

Biotechnology advances·2026
Same author

Differential diagnosis between oral squamous cell carcinoma and osteomyelitis through mandibular canal changes on panoramic radiographs.

BMC oral health·2026

Alzheimer's disease (AD) involves brain mitochondrial dysfunction. This study identified specific protein changes in AD mitochondria, revealing altered electron transport chain complexes as key drivers of AD pathology.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Gerontology

Background:

  • Mitochondrial dysfunction is central to aging and neurodegenerative diseases like Alzheimer's disease (AD).
  • The precise molecular differences in brain mitochondria between AD and healthy aging are not fully understood.

Purpose of the Study:

  • To identify AD-specific mitochondrial proteomic signatures.
  • To differentiate pathological changes in AD from normal aging processes in brain mitochondria.

Main Methods:

  • Utilized isobaric tag for relative and absolute quantitation (iTRAQ) and label-free quantitative proteomics.
  • Analyzed mitochondrial proteomes from human brain tissues of healthy individuals and AD patients.
  • Employed liquid chromatography-tandem mass spectrometry (LC-MS/MS) for proteomic profiling.
Keywords:
Alzheimer’s diseaseComplex IMitochondrial dysfunctionMitochondriomeNeurodegenerative diseasesProteomicsiTRAQ

Related Experiment Videos

Main Results:

  • Quantitative proteomics revealed distinct mitochondrial alterations in AD compared to healthy aging.
  • Dysregulation of electron transport chain (ETC) complexes and ATP-synthase were identified as potential drivers of AD pathology.
  • Specific subunits of ETC complex I (NDUFA4, NDUFA9) were altered in AD, indicating destabilization impacting mitochondrial function.

Conclusions:

  • Brain mitochondrial proteomes differ significantly between healthy aging and Alzheimer's disease.
  • Altered mitochondrial complexes, particularly electron transport chain complex I, are implicated in AD pathophysiology.
  • Proteomic analysis provides insights into the molecular basis of AD-specific mitochondrial dysfunction.