Topic: Amyloid, tau and blood-test diagnosis
Resumen Introducción La vía amiloidogénica de procesamiento de la proteína precursora del amiloide es bien conocida a nivel de patogenia y terapéutica en la enfermedad de Alzheimer (EA), mientras que la vía no-amiloidogénica ha sido menos estudiada. ADAM10 es la principal α-secretasa responsable de esta vía en el cerebro humano. Desarrollo ADAM10 pertenece a una familia de proteínas transmembrana con actividad catalítica. Actúa como α-secretasa sobre la proteína precursora del amiloide y otros muchos sustratos, algunos de ellos especialmente relevantes en el SNC. El gen ADAM10 ha sido señalado en estudios GWAS de EA; se han comunicado mutaciones en agregados familiares con respaldo funcional consistente pero segregación incompleta; y se ha demostrado el efecto de haploinsuficiencia de una mutación nonsense en una familia. Sin embargo, estudios genéticos de cohortes con EA no han encontrado variantes causales. Los niveles de ADAM10 en fluidos biológicos muestran resultados contradictorios excepto en plaquetas, donde los pacientes con EA tienen una reducción consistente. La estimulación de ADAM10 como diana terapéutica plantea posibilidades de desarrollo a través de varios componentes y medidas como el ejercicio físico, pero hasta ahora hay un solo ensayo clínico (positivo) con el retinoide acitretino. Conclusiones ADAM10 tiene un papel fundamental en el funcionamiento cerebral y suficientes estudios apoyan su implicación en la patogenia de la EA. Como causa genética hay solo ejemplos puntuales pero que animan a continuar su cribado en la EA familiar. Los niveles de ADAM10 en plaquetas podrían plantearse como biomarcador. La potenciación de ADAM10 en la EA es una diana terapéutica pendiente de más investigación.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Agüero, P., & Tortosa, E. G. (2026). ADAM10 y su implicación en la enfermedad de Alzheimer. Neurología. https://doi.org/10.1016/j.nrl.2026.502083
Vancouver
Agüero P, Tortosa EG. ADAM10 y su implicación en la enfermedad de Alzheimer. Neurología. 2026. doi:10.1016/j.nrl.2026.502083.
BibTeX
@article{aguero2026-69a3b153,
author = {Agüero, P. and Tortosa, E. Gómez},
title = {{ADAM10 y su implicación en la enfermedad de Alzheimer}},
journal = {Neurología},
year = {2026},
doi = {10.1016/j.nrl.2026.502083},
url = {https://doi.org/10.1016/j.nrl.2026.502083}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- La estimulación de ADAM10 como diana terapéutica plantea posibilidades de desarrollo a través de varios componentes y medidas como el ejercicio físico, pero hasta ahora hay un solo ensayo clínico (positivo) con el retinoide acitretino.
- Conclusiones ADAM10 tiene un papel fundamental en el funcionamiento cerebral y suficientes estudios apoyan su implicación en la patogenia de la EA.
- Como causa genética hay solo ejemplos puntuales pero que animan a continuar su cribado en la EA familiar.
- Los niveles de ADAM10 en plaquetas podrían plantearse como biomarcador.
- La potenciación de ADAM10 en la EA es una diana terapéutica pendiente de más investigación.
Why it matters
ADAM10 is the main α-secretase in the non-amyloidogenic pathway and is implicated in Alzheimer's pathogenesis, but genetic studies have not found causal variants in cohorts. Stimulating ADAM10 is a therapeutic possibility, with only one positive clinical trial using the retinoid acitretin so far.
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Study details
- Evidence strengthLow
How this study scored 27/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on senior author's track record, so that was left out: it earned 26 of the 96 points we could judge it on, which is 27 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurología) |
| Journal's citation record | 0 / 4 | Neurología: journal h-index 54 (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 | 5 / 5 | 2026 — within 1 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 0 / 7 | Cited 0 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.0 citations a year over 2 year(s) since 2026 |
| Impact for its field and year | 0 / 6 | Cited 0.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 0 / 4 | Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | OpenAlex's profile for last-listed author E. Gómez Tortosa holds only 6 work(s), too few to judge a track record — left out of this score |
| Institution's track record | 0 / 3 | Hospital Universitario Fundación Jiménez Díaz: institution h-index 301 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 2 / 2 | Free to read |
| Points | 26 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 26 of the 96 points we could judge it on is 27 out of 100. |
| Total | 27 / 100 | — |
What each of these 20 components measures, and what this score is not →
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