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The cell biology of beta-amyloid precursor protein and presenilin in Alzheimer's disease
Selkoe DJ.. Trends in cell biology, 1998-11-01
Topic: Disease mechanisms in lab and animal studies
It is a truism of modern biomedical science that the development of therapies expected to slow or arrest the progression of a disease requires as detailed an understanding of its molecular and cellular pathogenesis as possible. In turn, the cloning of novel gene products implicated in a disease often leads to new insights about fundamental features of protein structure and function. A particularly compelling example of this beneficial interplay between basic and applied cell biology arises from the exciting recent progress in deciphering Alzheimer's disease (AD). This review discusses the current understanding of the cell biology of two proteins crucial for the pathogenesis of AD, the beta-amyloid precursor protein and presenilin.
Key findings
- It is a truism of modern biomedical science that the development of therapies expected to slow or arrest the progression of a disease requires as detailed an understanding of its molecular and cellular pathogenesis as possible.
- In turn, the cloning of novel gene products implicated in a disease often leads to new insights about fundamental features of protein structure and function.
- A particularly compelling example of this beneficial interplay between basic and applied cell biology arises from the exciting recent progress in deciphering Alzheimer's disease (AD).
- This review discusses the current understanding of the cell biology of two proteins crucial for the pathogenesis of AD, the beta-amyloid precursor protein and presenilin.
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Study details
- Evidence strengthLow
How this study scored 36/100
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 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Trends in cell biology) |
| 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 | 1998 — older than 20 years, still counted |
| 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 9854312) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
What each of these 20 components measures, and what this score is not →
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APA 7th
Selkoe, D. J. (1998). The cell biology of beta-amyloid precursor protein and presenilin in Alzheimer's disease. Trends in cell biology. https://doi.org/10.1016/s0962-8924(98)01363-4
Vancouver
Selkoe DJ. The cell biology of beta-amyloid precursor protein and presenilin in Alzheimer's disease. Trends in cell biology. 1998. doi:10.1016/s0962-8924(98)01363-4. PMID: 9854312.
BibTeX
@article{selkoe1998-9854312,
author = {Selkoe, D. J.},
title = {{The cell biology of beta-amyloid precursor protein and presenilin in Alzheimer's disease}},
journal = {Trends in cell biology},
year = {1998},
doi = {10.1016/s0962-8924(98)01363-4},
pmid = {9854312},
url = {https://doi.org/10.1016/s0962-8924(98)01363-4}
}