Home › Research › Disease mechanisms
Interplay Between Mitochondrial Oxidative Disorders and Proteostasis in Alzheimer's Disease
Emilio Llanos-González, Ángel Andres Henares-Chavarino, Cristina María Pedrero-Prieto, Sonia García-Carpintero, Javier Frontiñán-Rubio, Francisco Javier Sancho-Bielsa, Francisco Javier Alcain, Juan Ramón Peinado et al.. Frontiers in neuroscience, 2020-01-29
Topic: Disease mechanisms in lab and animal studies
Although the basis of Alzheimer's disease (AD) etiology remains unknown, oxidative stress (OS) has been recognized as a prodromal factor associated to its progression. OS refers to an imbalance between oxidant and antioxidant systems, which usually consist in an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) which overwhelms the intrinsic antioxidant defenses. Due to this increased production of ROS and RNS, several biological functions such as glucose metabolism or synaptic activity are impaired. In AD, growing evidence links the ROS-mediated damages with molecular targets including mitochondrial dynamics and function, protein quality control system, and autophagic pathways, affecting the proteostasis balance. In this scenario, OS should be considered as not only a major feature in the pathophysiology of AD but also a potential target to combat the progression of the disease. In this review, we will discuss the role of OS in mitochondrial dysfunction, protein quality control systems, and autophagy associated to AD and suggest innovative therapeutic strategies based on a better understanding of the role of OS and proteostasis.
Key findings
- OS refers to an imbalance between oxidant and antioxidant systems, which usually consist in an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) which overwhelms the intrinsic antioxidant defenses.
- Due to this increased production of ROS and RNS, several biological functions such as glucose metabolism or synaptic activity are impaired.
- In AD, growing evidence links the ROS-mediated damages with molecular targets including mitochondrial dynamics and function, protein quality control system, and autophagic pathways, affecting the proteostasis balance.
- In this scenario, OS should be considered as not only a major feature in the pathophysiology of AD but also a potential target to combat the progression of the disease.
- In this review, we will discuss the role of OS in mitochondrial dysfunction, protein quality control systems, and autophagy associated to AD and suggest innovative therapeutic strategies based on a better understanding of the role of OS and proteostasis.
Study details
- Evidence strengthLow
How this study scored 39/100
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, multi-centre collaboration and free to read, so those were left out: it earned 22 of the 56 points we could judge it on, which is 39 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in neuroscience) |
| 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 32063825) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 22 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 22 of the 56 points we could judge it on is 39 out of 100. |
| Total | 39 / 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.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
APA 7th
Llanos-González, E., Henares-Chavarino, Á. A., Pedrero-Prieto, C. M., García-Carpintero, S., Frontiñán-Rubio, J., Sancho-Bielsa, F. J., et al. (2019). Interplay Between Mitochondrial Oxidative Disorders and Proteostasis in Alzheimer's Disease. Frontiers in neuroscience. https://doi.org/10.3389/fnins.2019.01444
Vancouver
Llanos-González E, Henares-Chavarino ÁA, Pedrero-Prieto CM, García-Carpintero S, Frontiñán-Rubio J, Sancho-Bielsa FJ, et al. Interplay Between Mitochondrial Oxidative Disorders and Proteostasis in Alzheimer's Disease. Frontiers in neuroscience. 2019. doi:10.3389/fnins.2019.01444. PMID: 32063825.
BibTeX
@article{llanosgonzalez2019-32063825,
author = {Llanos-González, Emilio and Henares-Chavarino, Ángel Andres and Pedrero-Prieto, Cristina María and García-Carpintero, Sonia and Frontiñán-Rubio, Javier and Sancho-Bielsa, Francisco Javier and Alcain, Francisco Javier and Peinado, Juan Ramón and others},
title = {{Interplay Between Mitochondrial Oxidative Disorders and Proteostasis in Alzheimer's Disease}},
journal = {Frontiers in neuroscience},
year = {2019},
doi = {10.3389/fnins.2019.01444},
pmid = {32063825},
url = {https://doi.org/10.3389/fnins.2019.01444}
}
Related studies in Disease mechanisms
Also tagged “mitochondrial”
275 studies in the library carry the topic tag “mitochondrial”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 275 tagged studies.