Quantitative profiling brain proteomes revealed mitochondrial dysfunction in Alzheimer's disease
Adav SS, Park JE, Sze SK, Sze SK.. Molecular brain, 2019-01-28
Topic: Amyloid, tau and blood-test diagnosis
Mitochondrial dysfunction is a key feature in both aging and neurodegenerative diseases including Alzheimer's disease (AD), but the molecular signature that distinguishes pathological changes in the AD from healthy aging in the brain mitochondria remain poorly understood. In order to unveil AD specific mitochondrial dysfunctions, this study adopted a discovery-driven approach with isobaric tag for relative and absolute quantitation (iTRAQ) and label-free quantitative proteomics, and profiled the mitochondrial proteomes in human brain tissues of healthy and AD individuals. LC-MS/MS-based iTRAQ quantitative proteomics approach revealed differentially altered mitochondriomes that distinguished the AD's pathophysiology-induced from aging-associated changes. Our results showed that dysregulated mitochondrial complexes including electron transport chain (ETC) and ATP-synthase are the potential driver for pathology of the AD. The iTRAQ results were cross-validated with independent label-free quantitative proteomics experiments to confirm that the subunit of electron transport chain complex I, particularly NDUFA4 and NDUFA9 were altered in AD patients, suggesting destabilization of the junction between membrane and matrix arms of mitochondrial complex I impacted the mitochondrial functions in the AD. iTRAQ quantitative proteomics of brain mitochondriomes revealed disparity in healthy aging and age-dependent AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Adav, S. S., Park, J. E., & Sze, S. K. (2019). Quantitative profiling brain proteomes revealed mitochondrial dysfunction in Alzheimer's disease. Molecular brain. https://doi.org/10.1186/s13041-019-0430-y
Vancouver
Adav SS, Park JE, Sze SK. Quantitative profiling brain proteomes revealed mitochondrial dysfunction in Alzheimer's disease. Molecular brain. 2019. doi:10.1186/s13041-019-0430-y. PMID: 30691479.
BibTeX
@article{adav2019-30691479,
author = {Adav, S. S. and Park, J. E. and Sze, S. K.},
title = {{Quantitative profiling brain proteomes revealed mitochondrial dysfunction in Alzheimer's disease}},
journal = {Molecular brain},
year = {2019},
doi = {10.1186/s13041-019-0430-y},
pmid = {30691479},
url = {https://doi.org/10.1186/s13041-019-0430-y}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- LC-MS/MS-based iTRAQ quantitative proteomics approach revealed differentially altered mitochondriomes that distinguished the AD's pathophysiology-induced from aging-associated changes.
- Our results showed that dysregulated mitochondrial complexes including electron transport chain (ETC) and ATP-synthase are the potential driver for pathology of the AD.
- The iTRAQ results were cross-validated with independent label-free quantitative proteomics experiments to confirm that the subunit of electron transport chain complex I, particularly NDUFA4 and NDUFA9 were altered in AD patients, suggesting destabilization of the junction between membrane and matrix arms of mitochondrial complex I impacted the mitochondrial functions in the AD. iTRAQ quantitative proteomics of brain mitochondriomes revealed disparity in healthy aging and age-dependent AD.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 41/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 24 of the 58 points we could judge it on, which is 41 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular brain) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2019 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 30691479) |
| Free to read | 2 / 2 | Free to read |
| Points | 24 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 24 of the 58 points we could judge it on is 41 out of 100. |
| Total | 41 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.
Related studies in Genetics
Also tagged “brain-proteome”
3 studies in the library carry the topic tag “brain-proteome”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 3 tagged studies.