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Aβ-induced acceleration of Alzheimer-related τ-pathology spreading and its association with prion protein
Gomes LA, Hipp SA, Rijal Upadhaya A, Balakrishnan K, Ospitalieri S, Koper MJ, Largo-Barrientos P, Uytterhoeven V et al.. Acta neuropathologica, 2019-08-14
Topic: Amyloid, tau and blood-test diagnosis
Extracellular deposition of amyloid β-protein (Aβ) in amyloid plaques and intracellular accumulation of abnormally phosphorylated τ-protein (p-τ) in neurofibrillary tangles (NFTs) represent pathological hallmark lesions of Alzheimer's disease (AD). Both lesions develop in parallel in the human brain throughout the preclinical and clinical course of AD. Nevertheless, it is not yet clear whether there is a direct link between Aβ and τ pathology or whether other proteins are involved in this process.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Gomes, L. A., Hipp, S. A., Rijal Upadhaya, A., Balakrishnan, K., Ospitalieri, S., Koper, M. J., et al. (2019). Aβ-induced acceleration of Alzheimer-related τ-pathology spreading and its association with prion protein. Acta neuropathologica. https://doi.org/10.1007/s00401-019-02053-5
Vancouver
Gomes LA, Hipp SA, Rijal Upadhaya A, Balakrishnan K, Ospitalieri S, Koper MJ, et al. Aβ-induced acceleration of Alzheimer-related τ-pathology spreading and its association with prion protein. Acta neuropathologica. 2019. doi:10.1007/s00401-019-02053-5. PMID: 31414210.
BibTeX
@article{gomes2019-31414210,
author = {Gomes, L. A. and Hipp, S. A. and Rijal Upadhaya, A. and Balakrishnan, K. and Ospitalieri, S. and Koper, M. J. and Largo-Barrientos, P. and Uytterhoeven, V. and others},
title = {{Aβ-induced acceleration of Alzheimer-related τ-pathology spreading and its association with prion protein}},
journal = {Acta neuropathologica},
year = {2019},
doi = {10.1007/s00401-019-02053-5},
pmid = {31414210},
url = {https://doi.org/10.1007/s00401-019-02053-5}
}
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Key findings
- Both lesions develop in parallel in the human brain throughout the preclinical and clinical course of AD.
- Nevertheless, it is not yet clear whether there is a direct link between Aβ and τ pathology or whether other proteins are involved in this process.
- To address this question, we crossed amyloid precursor protein (APP) transgenic mice overexpressing human APP with the Swedish mutation (670/671 KM → NL) (APP23), human wild-type APP (APP51/16), or a proenkephalin signal peptide linked to human Aβ 42 (APP48) with τ-transgenic mice overexpressing human mutant 4-repeat τ-protein with the P301S mutation (TAU58).
- In 6-month-old APP23xTAU58 and APP51/16xTAU58 mice, soluble Aβ was associated with the aggravation of p-τ pathology propagation into the CA1/subiculum region, whereas 6-month-old TAU58 and APP48xTAU58 mice neither exhibited significant amounts of p-τ pathology in the CA1/subiculum region nor displayed significant levels of soluble Aβ in the forebrain.
Why it matters
Using crossed transgenic mouse models, this study examined whether amyloid β accelerates the spread of tau pathology and how prion protein may be involved. It is animal research and does not show a treatment, cure, or prevention for people.
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Study details
- Evidence strengthLow
How this study scored 50/100
Published in a leading specialty journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Acta neuropathologica) |
| Journal's citation record | 3 / 4 | Acta Neuropathologica: journal h-index 287 (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 | 2 / 5 | 2019 — 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 126 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 14.0 citations a year over 9 year(s) since 2019 |
| Impact for its field and year | 4 / 6 | Cited 10.0× 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 43 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Dietmar Rudolf Thal: h-index 84 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | KU Leuven: institution h-index 1,386 (OpenAlex) |
| Multicenter collaboration | 3 / 3 | OpenAlex lists 12 institution(s) in 3 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 31414210) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 50 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1007/s00401-019-02053-5
- PubMed: 31414210
- Original source →
- Free full text: Lirias (KU Leuven) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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