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Endoplasmic reticulum stress mediates amyloid β neurotoxicity via mitochondrial cholesterol trafficking
Barbero-Camps E, Fernández A, Baulies A, Martinez L, Fernández-Checa JC, Colell A.. The American journal of pathology, 2014-05-09
Topic: Brain proteins, microglia and lab models
Disrupted cholesterol homeostasis has been reported in Alzheimer disease and is thought to contribute to disease progression by promoting amyloid β (Aβ) accumulation. In particular, mitochondrial cholesterol enrichment has been shown to sensitize to Aβ-induced neurotoxicity. However, the molecular mechanisms responsible for the increased cholesterol levels and its trafficking to mitochondria in Alzheimer disease remain poorly understood.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Barbero-Camps, E., Fernández, A., Baulies, A., Martinez, L., Fernández-Checa, J. C., & Colell, A. (2014). Endoplasmic reticulum stress mediates amyloid β neurotoxicity via mitochondrial cholesterol trafficking. The American journal of pathology. https://doi.org/10.1016/j.ajpath.2014.03.014
Vancouver
Barbero-Camps E, Fernández A, Baulies A, Martinez L, Fernández-Checa JC, Colell A. Endoplasmic reticulum stress mediates amyloid β neurotoxicity via mitochondrial cholesterol trafficking. The American journal of pathology. 2014. doi:10.1016/j.ajpath.2014.03.014. PMID: 24815354.
BibTeX
@article{barberocamps2014-24815354,
author = {Barbero-Camps, E. and Fernández, A. and Baulies, A. and Martinez, L. and Fernández-Checa, J. C. and Colell, A.},
title = {{Endoplasmic reticulum stress mediates amyloid β neurotoxicity via mitochondrial cholesterol trafficking}},
journal = {The American journal of pathology},
year = {2014},
doi = {10.1016/j.ajpath.2014.03.014},
pmid = {24815354},
url = {https://doi.org/10.1016/j.ajpath.2014.03.014}
}
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Key findings
- In particular, mitochondrial cholesterol enrichment has been shown to sensitize to Aβ-induced neurotoxicity.
- However, the molecular mechanisms responsible for the increased cholesterol levels and its trafficking to mitochondria in Alzheimer disease remain poorly understood.
- Here, we show that endoplasmic reticulum (ER) stress triggered by Aβ promotes cholesterol synthesis and mitochondrial cholesterol influx, resulting in mitochondrial glutathione (mGSH) depletion in older age amyloid precursor protein/presenilin-1 (APP/PS1) mice.
- Mitochondrial cholesterol accumulation was associated with increased expression of mitochondrial-associated ER membrane proteins, which favor cholesterol translocation from ER to mitochondria along with specific cholesterol carriers, particularly the steroidogenic acute regulatory protein.
Why it matters
This study shows that endoplasmic reticulum stress triggered by amyloid beta promotes cholesterol synthesis and mitochondrial cholesterol influx, resulting in mitochondrial glutathione depletion in older age amyloid precursor protein mice. It is mechanistic work in a mouse model and does not show that targeting this process treats, cures or prevents Alzheimer's disease in people.
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Study details
- Evidence strengthLow
How this study scored 45/100
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 (The American journal of pathology) |
| Journal's citation record | 3 / 4 | American Journal Of Pathology: journal h-index 328 (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 | 1 / 5 | 2014 — within 20 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 104 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 7.4 citations a year over 14 year(s) since 2014 |
| Impact for its field and year | 3 / 6 | Cited 5.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | 2 / 4 | Cited 19 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Anna Colell: h-index 59 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Southern California: institution h-index 1,521 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 24815354) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.ajpath.2014.03.014
- PubMed: 24815354
- Original source →
- Free full text: American Journal Of Pathology →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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