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Striatal amyloid is associated with tauopathy and memory decline in familial Alzheimer's disease
Hanseeuw BJ, Lopera F, Sperling RA, Norton DJ, Guzman-Velez E, Baena A, Pardilla-Delgado E, Schultz AP et al.. Alzheimer's research & therapy, 2019-02-04
Topic: Amyloid, tau and blood-test diagnosis
Background Autosomal dominant Alzheimer's disease (ADAD) is distinguished from late-onset AD by early striatal amyloid-β deposition. To determine whether striatal Pittsburgh compound B (PiB)-PET measurements of amyloid-β can help predict disease severity in ADAD, we compared relationships of striatal and neocortical PiB-PET to age, tau-PET, and memory performance in the Colombian Presenilin 1 E280A kindred. Methods Fourteen carriers (age = 28-42, Mini-Mental State Examination = 26-30) and 20 age-matched non-carriers were evaluated using PiB, flortaucipir (FTP; tau), and memory testing (CERAD Word List Learning). PiB-PET signal was measured in neocortical and striatal aggregates. FTP-PET signal was measured in entorhinal cortex. Results Compared to non-carriers, mutation carriers had age-related elevations in both neocortical and striatal PiB binding. The PiB elevation in carriers was significantly greater in the striatum than in the neocortex. In mutation carriers, PiB binding in both the neocortex and the striatum is related to entorhinal FTP; however, the association was stronger with the striatum. Only striatal PiB was associated with worse memory. Remarkably, PiB binding in the striatum, but not in the neocortex, predicted entorhinal FTP and lower memory scores after adjusting for age, indicating that striatal PiB identified the carriers with the most severe disease. Conclusions Based on these preliminary cross-sectional findings, striatal PiB-PET measurements may offer particular value in the detection and tracking of preclinical ADAD, informing a mutation carrier's prognosis and evaluating amyloid-β-modifying ADAD treatments.
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APA 7th
Hanseeuw, B. J., Lopera, F., Sperling, R. A., Norton, D. J., Guzman-Velez, E., Baena, A., et al. (2019). Striatal amyloid is associated with tauopathy and memory decline in familial Alzheimer's disease. Alzheimer's research & therapy. https://doi.org/10.1186/s13195-019-0468-1
Vancouver
Hanseeuw BJ, Lopera F, Sperling RA, Norton DJ, Guzman-Velez E, Baena A, et al. Striatal amyloid is associated with tauopathy and memory decline in familial Alzheimer's disease. Alzheimer's research & therapy. 2019. doi:10.1186/s13195-019-0468-1. PMID: 30717814.
BibTeX
@article{hanseeuw2019-30717814,
author = {Hanseeuw, B. J. and Lopera, F. and Sperling, R. A. and Norton, D. J. and Guzman-Velez, E. and Baena, A. and Pardilla-Delgado, E. and Schultz, A. P. and others},
title = {{Striatal amyloid is associated with tauopathy and memory decline in familial Alzheimer's disease}},
journal = {Alzheimer's research \& therapy},
year = {2019},
doi = {10.1186/s13195-019-0468-1},
pmid = {30717814},
url = {https://doi.org/10.1186/s13195-019-0468-1}
}
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Key findings
- Results Compared to non-carriers, mutation carriers had age-related elevations in both neocortical and striatal PiB binding.
- The PiB elevation in carriers was significantly greater in the striatum than in the neocortex.
- Only striatal PiB was associated with worse memory.
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Study details
- Study designcross-sectional
- Evidence strengthLow
How this study scored 48/100
Published in a peer-reviewed journal, and it is a snapshot of people at one point in time. Scored zero for 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 28 of the 58 points we could judge it on, which is 48 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Alzheimer's research & therapy) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 4 / 12 | A snapshot of people at one point in time |
| 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) |
| 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 30717814) |
| Free to read | 2 / 2 | Free to read |
| Points | 28 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 28 of the 58 points we could judge it on is 48 out of 100. |
| Total | 48 / 100 | — |
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