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Basal forebrain degeneration precedes and predicts the cortical spread of Alzheimer’s pathology
Taylor W. Schmitz, R. Nathan Spreng, The Alzheimer's Disease Neuroimaging Initiative, Michael Walter Weiner, Paul S. S Aisen, Ronald Carl Petersen, Clifford R. Jack, William J. Jagust et al.. Nature Communications, 2016-11-04
Topic: Brain imaging, connectivity and assessment
There is considerable debate whether Alzheimer's disease (AD) originates in basal forebrain or entorhinal cortex. Here we examined whether longitudinal decreases in basal forebrain and entorhinal cortex grey matter volume were interdependent and sequential. In a large cohort of age-matched older adults ranging from cognitively normal to AD, we demonstrate that basal forebrain volume predicts longitudinal entorhinal degeneration. Models of parallel degeneration or entorhinal origin received negligible support. We then integrated volumetric measures with an amyloid biomarker sensitive to pre-symptomatic AD pathology. Comparison between cognitively matched normal adult subgroups, delineated according to the amyloid biomarker, revealed abnormal degeneration in basal forebrain, but not entorhinal cortex. Abnormal degeneration in both basal forebrain and entorhinal cortex was only observed among prodromal (mildly amnestic) individuals. We provide evidence that basal forebrain pathology precedes and predicts both entorhinal pathology and memory impairment, challenging the widely held belief that AD has a cortical origin.
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APA 7th
Schmitz, T. W., Spreng, R. N., The Alzheimer's Disease Neuroimaging Initiative, Weiner, M. W., Aisen, P. S. S., Petersen, R. C., et al. (2016). Basal forebrain degeneration precedes and predicts the cortical spread of Alzheimer’s pathology. Nature Communications. https://doi.org/10.1038/ncomms13249
Vancouver
Schmitz TW, Spreng RN, The Alzheimer's Disease Neuroimaging Initiative, Weiner MW, Aisen PSS, Petersen RC, et al. Basal forebrain degeneration precedes and predicts the cortical spread of Alzheimer’s pathology. Nature Communications. 2016. doi:10.1038/ncomms13249. PMID: 27811848.
BibTeX
@article{schmitz2016-27811848,
author = {Schmitz, Taylor W. and Spreng, R. Nathan and {The Alzheimer's Disease Neuroimaging Initiative} and Weiner, Michael Walter and Aisen, Paul S. S and Petersen, Ronald Carl and Jack, Clifford R. and Jagust, William J. and others},
title = {{Basal forebrain degeneration precedes and predicts the cortical spread of Alzheimer’s pathology}},
journal = {Nature Communications},
year = {2016},
doi = {10.1038/ncomms13249},
pmid = {27811848},
url = {https://doi.org/10.1038/ncomms13249}
}
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Key findings
- Comparison between cognitively matched normal adult subgroups, delineated according to the amyloid biomarker, revealed abnormal degeneration in basal forebrain, but not entorhinal cortex.
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Study details
- Study designlongitudinal study
- Evidence strengthModerate
How this study scored 59/100
Published in a leading specialty journal, and it is a longitudinal study following the same people over 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 34 of the 58 points we could judge it on, which is 59 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Nature Communications) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 7 / 12 | A longitudinal study following the same people over time |
| Strength of evidence | 3 / 5 | Rated “moderate” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2016 — within 20 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 27811848) |
| Free to read | 2 / 2 | Free to read |
| Points | 34 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 34 of the 58 points we could judge it on is 59 out of 100. |
| Total | 59 / 100 | — |
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