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Spatially distinct atrophy is linked to β-amyloid and tau in preclinical Alzheimer disease
Wang L, Benzinger TL, Hassenstab J, Blazey T, Owen C, Liu J, Fagan AM, Morris JC et al.. Neurology, 2015-02-25
Topic: Amyloid, tau and blood-test diagnosis
Objectives To determine whether an MRI-based Alzheimer disease (AD) signature biomarker can detect tau-related neurodegeneration in preclinical AD, and to assess whether AD signature cortical thinning is associated with cognitive changes in cognitively normal (CN) older individuals. Methods In a large cohort of CN individuals (n = 188), we measured the hippocampal volume and cortical thickness within independently defined AD signature regions. We cross-sectionally assessed the associations between AD signature cortical thinning or hippocampal atrophy with CSF biomarkers of tau (increased tau) and β-amyloid (Aβ) (decreased Aβ42). We also examined the impact of AD signature cortical thinning or other biomarker changes (i.e., hippocampal atrophy, reduced CSF Aβ42, or increased CSF tau) on cognitive performance in CN individuals. Results Elevated CSF tau was associated with AD signature cortical thinning but not hippocampal atrophy. In contrast, decreased CSF Aβ42 was associated with hippocampal loss but not AD signature cortical thinning. In addition, AD signature cortical thinning was associated with lower visuospatial performance. Reduced CSF Aβ42 was related to poorer performance on episodic memory. Conclusions Spatially distinct neurodegeneration is associated with Aβ and tau pathology in preclinical AD. Aβ deposition and AD signature cortical atrophy independently affect cognition in CN older individuals.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Wang, L., Benzinger, T. L., Hassenstab, J., Blazey, T., Owen, C., Liu, J., et al. (2015). Spatially distinct atrophy is linked to β-amyloid and tau in preclinical Alzheimer disease. Neurology. https://doi.org/10.1212/wnl.0000000000001401
Vancouver
Wang L, Benzinger TL, Hassenstab J, Blazey T, Owen C, Liu J, et al. Spatially distinct atrophy is linked to β-amyloid and tau in preclinical Alzheimer disease. Neurology. 2015. doi:10.1212/wnl.0000000000001401. PMID: 25716355.
BibTeX
@article{wang2015-25716355,
author = {Wang, L. and Benzinger, T. L. and Hassenstab, J. and Blazey, T. and Owen, C. and Liu, J. and Fagan, A. M. and Morris, J. C. and others},
title = {{Spatially distinct atrophy is linked to β-amyloid and tau in preclinical Alzheimer disease}},
journal = {Neurology},
year = {2015},
doi = {10.1212/wnl.0000000000001401},
pmid = {25716355},
url = {https://doi.org/10.1212/wnl.0000000000001401}
}
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Key findings
- Objectives To determine whether an MRI-based Alzheimer disease (AD) signature biomarker can detect tau-related neurodegeneration in preclinical AD, and to assess whether AD signature cortical thinning is associated with cognitive changes in cognitively normal (CN) older individuals.
- Results Elevated CSF tau was associated with AD signature cortical thinning but not hippocampal atrophy.
- In contrast, decreased CSF Aβ42 was associated with hippocampal loss but not AD signature cortical thinning.
- In addition, AD signature cortical thinning was associated with lower visuospatial performance.
- Conclusions Spatially distinct neurodegeneration is associated with Aβ and tau pathology in preclinical AD.
Why it matters
In 188 cognitively normal older individuals, elevated CSF tau was associated with cortical thinning in Alzheimer disease signature regions but not hippocampal atrophy, while decreased CSF β-amyloid 42 was associated with hippocampal loss but not cortical thinning. This describes how two pathologies relate to different brain changes in preclinical Alzheimer's disease, not a treatment or cure.
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Study details
- Participants188
- Evidence strengthModerate
How this study scored 50/100
Published in a leading specialty journal. Scored zero for study design, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Neurology) |
| Journal's citation record | 4 / 4 | Neurology: journal h-index 525 (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 | 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 | 2015 — within 20 year(s) of the newest study here |
| Sample size | 2 / 4 | 188 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 79 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 6.1 citations a year over 13 year(s) since 2015 |
| Impact for its field and year | 3 / 6 | Cited 6.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 11 other studies in this library |
| Still being cited | 1 / 4 | Cited 14 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Beau M. Ances: h-index 81 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Hope Center for Neurological Disorders: institution h-index 354 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 25716355) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 50 / 100 | — |
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