The Endosomal-Lysosomal Pathway Is Dysregulated by APOE4 Expression in Vivo
Nuriel T, Peng KY, Ashok A, Dillman AA, Figueroa HY, Apuzzo J, Ambat J, Levy E et al.. Frontiers in neuroscience, 2017-12-12
Topic: Brain proteins, microglia and lab models
Possession of the ε4 allele of apolipoprotein E ( APOE ) is the major genetic risk factor for late-onset Alzheimer's disease (AD). Although numerous hypotheses have been proposed, the precise cause of this increased AD risk is not yet known. In order to gain a more comprehensive understanding of APOE4 's role in AD, we performed RNA-sequencing on an AD-vulnerable vs. an AD-resistant brain region from aged APOE targeted replacement mice. This transcriptomics analysis revealed a significant enrichment of genes involved in endosomal-lysosomal processing, suggesting an APOE4 -specific endosomal-lysosomal pathway dysregulation in the brains of APOE4 mice. Further analysis revealed clear differences in the morphology of endosomal-lysosomal compartments, including an age-dependent increase in the number and size of early endosomes in APOE4 mice. These findings directly link the APOE4 genotype to endosomal-lysosomal dysregulation in an in vivo , AD pathology-free setting, which may play a causative role in the increased incidence of AD among APOE4 carriers.
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APA 7th
Nuriel, T., Peng, K. Y., Ashok, A., Dillman, A. A., Figueroa, H. Y., Apuzzo, J., et al. (2017). The Endosomal-Lysosomal Pathway Is Dysregulated by APOE4 Expression in Vivo. Frontiers in neuroscience. https://doi.org/10.3389/fnins.2017.00702
Vancouver
Nuriel T, Peng KY, Ashok A, Dillman AA, Figueroa HY, Apuzzo J, et al. The Endosomal-Lysosomal Pathway Is Dysregulated by APOE4 Expression in Vivo. Frontiers in neuroscience. 2017. doi:10.3389/fnins.2017.00702. PMID: 29311783.
BibTeX
@article{nuriel2017-29311783,
author = {Nuriel, T. and Peng, K. Y. and Ashok, A. and Dillman, A. A. and Figueroa, H. Y. and Apuzzo, J. and Ambat, J. and Levy, E. and others},
title = {{The Endosomal-Lysosomal Pathway Is Dysregulated by APOE4 Expression in Vivo}},
journal = {Frontiers in neuroscience},
year = {2017},
doi = {10.3389/fnins.2017.00702},
pmid = {29311783},
url = {https://doi.org/10.3389/fnins.2017.00702}
}
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Key findings
- This transcriptomics analysis revealed a significant enrichment of genes involved in endosomal-lysosomal processing, suggesting an APOE4 -specific endosomal-lysosomal pathway dysregulation in the brains of APOE4 mice.
- Further analysis revealed clear differences in the morphology of endosomal-lysosomal compartments, including an age-dependent increase in the number and size of early endosomes in APOE4 mice.
- These findings directly link the APOE4 genotype to endosomal-lysosomal dysregulation in an in vivo , AD pathology-free setting, which may play a causative role in the increased incidence of AD among APOE4 carriers.
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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 (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 | 2017 — 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 29311783) |
| 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 | — |
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