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Amyloid-β and hyperphosphorylated tau synergy drives metabolic decline in preclinical Alzheimer's disease
Pascoal TA, Mathotaarachchi S, Mohades S, Benedet AL, Chung CO, Shin M, Wang S, Beaudry T et al.. Molecular psychiatry, 2016-03-29
Topic: Amyloid, tau and blood-test diagnosis
This study was designed to test the interaction between amyloid-β and tau proteins as a determinant of metabolic decline in preclinical Alzheimer's disease (AD). We assessed 120 cognitively normal individuals with [ 18 F]florbetapir positron emission tomography (PET) and cerebrospinal fluid (CSF) measurements at baseline, as well as [ 18 F]fluorodeoxyglucose ([ 18 F]FDG) PET at baseline and at 24 months. A voxel-based interaction model was built to test the associations between continuous measurements of CSF biomarkers, [ 18 F]florbetapir and [ 18 F]FDG standardized uptake value ratios (SUVR). We found that the synergistic interaction between [ 18 F]florbetapir SUVR and CSF phosphorylated tau (p-tau) measurements, rather than the sum of their independent effects, was associated with a 24-month metabolic decline in basal and mesial temporal, orbitofrontal, and anterior and posterior cingulate cortices (P<0.001). In contrast, interactions using CSF amyloid-β 1-42 and total tau biomarkers did not associate with metabolic decline over a time frame of 24 months. The interaction found in this study further support the framework that amyloid-β and hyperphosphorylated tau aggregates synergistically interact to cause downstream AD neurodegeneration. In fact, the regions displaying the metabolic decline reported here were confined to brain networks affected early by amyloid-β plaques and neurofibrillary tangles. Preventive clinical trials may benefit from using a combination of amyloid-β PET and p-tau biomarkers to enrich study populations of cognitively normal subjects with a high probability of disease progression in studies, using [ 18 F]FDG as a biomarker of efficacy.
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APA 7th
Pascoal, T. A., Mathotaarachchi, S., Mohades, S., Benedet, A. L., Chung, C. O., Shin, M., et al. (2017). Amyloid-β and hyperphosphorylated tau synergy drives metabolic decline in preclinical Alzheimer's disease. Molecular psychiatry. https://doi.org/10.1038/mp.2016.37
Vancouver
Pascoal TA, Mathotaarachchi S, Mohades S, Benedet AL, Chung CO, Shin M, et al. Amyloid-β and hyperphosphorylated tau synergy drives metabolic decline in preclinical Alzheimer's disease. Molecular psychiatry. 2017. doi:10.1038/mp.2016.37. PMID: 27021814.
BibTeX
@article{pascoal2017-27021814,
author = {Pascoal, T. A. and Mathotaarachchi, S. and Mohades, S. and Benedet, A. L. and Chung, C. O. and Shin, M. and Wang, S. and Beaudry, T. and others},
title = {{Amyloid-β and hyperphosphorylated tau synergy drives metabolic decline in preclinical Alzheimer's disease}},
journal = {Molecular psychiatry},
year = {2017},
doi = {10.1038/mp.2016.37},
pmid = {27021814},
url = {https://doi.org/10.1038/mp.2016.37}
}
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Key findings
- We found that the synergistic interaction between [ 18 F]florbetapir SUVR and CSF phosphorylated tau (p-tau) measurements, rather than the sum of their independent effects, was associated with a 24-month metabolic decline in basal and mesial temporal, orbitofrontal, and anterior and posterior cingulate cortices (P<0.001).
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Study details
- Evidence strengthLow
How this study scored 45/100
Published in a leading specialty 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 26 of the 58 points we could judge it on, which is 45 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Molecular psychiatry) |
| 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 27021814) |
| Free to read | 2 / 2 | Free to read |
| Points | 26 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 26 of the 58 points we could judge it on is 45 out of 100. |
| Total | 45 / 100 | — |
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