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Extracellular Vesicle-Associated Aβ Mediates Trans-Neuronal Bioenergetic and Ca 2+ -Handling Deficits in Alzheimer's Disease Models
Eitan E, Hutchison ER, Marosi K, Comotto J, Mustapic M, Nigam SM, Suire C, Maharana C et al.. NPJ aging and mechanisms of disease, 2016-09-22
Topic: Disease mechanisms in lab and animal studies
Alzheimer's Disease (AD) is an age-related neurodegenerative disorder in which aggregation-prone neurotoxic amyloid β-peptide (Aβ) accumulates in the brain. Extracellular vesicles (EVs) are small 50-150 nanometer membrane vesicles that have recently been implicated in the prion-like spread of self-aggregating proteins. Here we report that EVs isolated from AD patient CSF and plasma, from the plasma of two AD mouse models, and from the medium of neural cells expressing familial AD presenilin 1 mutations, destabilize neuronal Ca 2+ homeostasis, impair mitochondrial function, and sensitize neurons to excitotoxicity. EVs contain a relatively low amount of Aβ but have an increased Aβ42/ Aβ40 ratio; the majority of Aβ is located on the surface of the EVs. Impairment of lysosome function results in increased generation EVs with elevated Aβ42 levels. EVs may mediate transcellular spread of pathogenic Aβ species and that impair neuronal Ca 2+ handling and mitochondrial function, and may thereby render neurons vulnerable to excitotoxicity.
Key findings
- Impairment of lysosome function results in increased generation EVs with elevated Aβ42 levels.
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Study details
- Evidence strengthLow
How this study scored 40/100
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 23 of the 58 points we could judge it on, which is 40 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (NPJ aging and mechanisms of disease) |
| 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 | 1 / 5 | 2016 — 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 | — / 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 27928512) |
| Free to read | 2 / 2 | Free to read |
| Points | 23 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 23 of the 58 points we could judge it on is 40 out of 100. |
| Total | 40 / 100 | — |
What each of these 20 components measures, and what this score is not →
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APA 7th
Eitan, E., Hutchison, E. R., Marosi, K., Comotto, J., Mustapic, M., Nigam, S. M., et al. (2016). Extracellular Vesicle-Associated Aβ Mediates Trans-Neuronal Bioenergetic and Ca 2+ -Handling Deficits in Alzheimer's Disease Models. NPJ aging and mechanisms of disease. https://doi.org/10.1038/npjamd.2016.19
Vancouver
Eitan E, Hutchison ER, Marosi K, Comotto J, Mustapic M, Nigam SM, et al. Extracellular Vesicle-Associated Aβ Mediates Trans-Neuronal Bioenergetic and Ca 2+ -Handling Deficits in Alzheimer's Disease Models. NPJ aging and mechanisms of disease. 2016. doi:10.1038/npjamd.2016.19. PMID: 27928512.
BibTeX
@article{eitan2016-27928512,
author = {Eitan, E. and Hutchison, E. R. and Marosi, K. and Comotto, J. and Mustapic, M. and Nigam, S. M. and Suire, C. and Maharana, C. and others},
title = {{Extracellular Vesicle-Associated Aβ Mediates Trans-Neuronal Bioenergetic and Ca 2+ -Handling Deficits in Alzheimer's Disease Models}},
journal = {NPJ aging and mechanisms of disease},
year = {2016},
doi = {10.1038/npjamd.2016.19},
pmid = {27928512},
url = {https://doi.org/10.1038/npjamd.2016.19}
}