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A key role for MAM in mediating mitochondrial dysfunction in Alzheimer disease
Area-Gomez E, de Groof A, Bonilla E, Montesinos J, Tanji K, Boldogh I, Pon L, Schon EA.. Cell death & disease, 2018-02-28
Topic: Amyloid, tau and blood-test diagnosis
In the last few years, increased emphasis has been devoted to understanding the contribution of mitochondria-associated endoplasmic reticulum (ER) membranes (MAM) to human pathology in general, and neurodegenerative diseases in particular. A major reason for this is the central role that this subdomain of the ER plays in metabolic regulation and in mitochondrial biology. As such, aberrant MAM function may help explain the seemingly unrelated metabolic abnormalities often seen in neurodegeneration.
Key findings
- A major reason for this is the central role that this subdomain of the ER plays in metabolic regulation and in mitochondrial biology.
- As such, aberrant MAM function may help explain the seemingly unrelated metabolic abnormalities often seen in neurodegeneration.
- In the specific case of Alzheimer disease (AD), besides perturbations in calcium and lipid homeostasis, there are numerous documented alterations in mitochondrial behavior and function, including reduced respiratory chain activity and oxidative phosphorylation, increased free radical production, and altered organellar morphology, dynamics, and positioning (especially perinuclear mitochondria).
- However, whether these alterations are primary events causative of the disease, or are secondary downstream events that are the result of some other, more fundamental problem, is still unclear.
Why it matters
This review discusses how altered mitochondria-associated ER membranes may explain metabolic abnormalities in Alzheimer's disease, including reduced respiratory chain activity. It proposes a possible mechanism but reports no treatment or cure.
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Study details
- Evidence strengthLow
How this study scored 49/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Cell death & disease) |
| Journal's citation record | 2 / 4 | Cell Death and Disease: journal h-index 233 (OpenAlex, 2026-10-29) |
| 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 | 2018 — 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 | 5 / 7 | Cited 232 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 23.2 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 4 / 6 | Cited 8.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 3 / 4 | Cited 71 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Eric A. Schon: h-index 95 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Columbia University: institution h-index 1,824 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 29491396) |
| Free to read | 2 / 2 | Free to read |
| Total | 49 / 100 | — |
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Read the original
- DOI: 10.1038/s41419-017-0215-0
- PubMed: 29491396
- Original source →
- Free full text: Cell Death and Disease →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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 names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
APA 7th
Area-Gomez, E., de Groof, A., Bonilla, E., Montesinos, J., Tanji, K., Boldogh, I., et al. (2018). A key role for MAM in mediating mitochondrial dysfunction in Alzheimer disease. Cell death & disease. https://doi.org/10.1038/s41419-017-0215-0
Vancouver
Area-Gomez E, de Groof A, Bonilla E, Montesinos J, Tanji K, Boldogh I, et al. A key role for MAM in mediating mitochondrial dysfunction in Alzheimer disease. Cell death & disease. 2018. doi:10.1038/s41419-017-0215-0. PMID: 29491396.
BibTeX
@article{areagomez2018-29491396,
author = {Area-Gomez, E. and de Groof, A. and Bonilla, E. and Montesinos, J. and Tanji, K. and Boldogh, I. and Pon, L. and Schon, E. A.},
title = {{A key role for MAM in mediating mitochondrial dysfunction in Alzheimer disease}},
journal = {Cell death \& disease},
year = {2018},
doi = {10.1038/s41419-017-0215-0},
pmid = {29491396},
url = {https://doi.org/10.1038/s41419-017-0215-0}
}
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