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Dendritic spines provide cognitive resilience against Alzheimer's disease
Boros BD, Greathouse KM, Gentry EG, Curtis KA, Birchall EL, Gearing M, Herskowitz JH.. Annals of neurology, 2017-10-22
Topic: Amyloid, tau and blood-test diagnosis
Objective Neuroimaging and other biomarker assays suggest that the pathological processes of Alzheimer's disease (AD) begin years prior to clinical dementia onset. However, some 30 to 50% of older individuals who harbor AD pathology do not become symptomatic in their lifetime. It is hypothesized that such individuals exhibit cognitive resilience that protects against AD dementia. We hypothesized that in cases with AD pathology, structural changes in dendritic spines would distinguish individuals who had or did not have clinical dementia. Methods We compared dendritic spines within layer II and III pyramidal neuron dendrites in Brodmann area 46 dorsolateral prefrontal cortex using the Golgi-Cox technique in 12 age-matched pathology-free controls, 8 controls with AD pathology (CAD), and 21 AD cases. We used highly optimized methods to trace impregnated dendrites from bright-field microscopy images that enabled accurate 3-dimensional digital reconstruction of dendritic structure for morphologic analyses. Results Spine density was similar among control and CAD cases but was reduced significantly in AD. Thin and mushroom spines were reduced significantly in AD compared to CAD brains, whereas stubby spine density was decreased significantly in CAD and AD compared to controls. Increased spine extent distinguished CAD cases from controls and AD. Linear regression analysis of all cases indicated that spine density was not associated with neuritic plaque score but did display negative correlation with Braak staging. Interpretation These observations provide cellular evidence to support the hypothesis that dendritic spine plasticity is a mechanism of cognitive resilience that protects older individuals with AD pathology from developing dementia. Ann Neurol 2017;82:602-614.
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APA 7th
Boros, B. D., Greathouse, K. M., Gentry, E. G., Curtis, K. A., Birchall, E. L., Gearing, M., et al. (2017). Dendritic spines provide cognitive resilience against Alzheimer's disease. Annals of neurology. https://doi.org/10.1002/ana.25049
Vancouver
Boros BD, Greathouse KM, Gentry EG, Curtis KA, Birchall EL, Gearing M, et al. Dendritic spines provide cognitive resilience against Alzheimer's disease. Annals of neurology. 2017. doi:10.1002/ana.25049. PMID: 28921611.
BibTeX
@article{boros2017-28921611,
author = {Boros, B. D. and Greathouse, K. M. and Gentry, E. G. and Curtis, K. A. and Birchall, E. L. and Gearing, M. and Herskowitz, J. H.},
title = {{Dendritic spines provide cognitive resilience against Alzheimer's disease}},
journal = {Annals of neurology},
year = {2017},
doi = {10.1002/ana.25049},
pmid = {28921611},
url = {https://doi.org/10.1002/ana.25049}
}
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Key findings
- Objective Neuroimaging and other biomarker assays suggest that the pathological processes of Alzheimer's disease (AD) begin years prior to clinical dementia onset.
- Results Spine density was similar among control and CAD cases but was reduced significantly in AD.
- Thin and mushroom spines were reduced significantly in AD compared to CAD brains, whereas stubby spine density was decreased significantly in CAD and AD compared to controls.
- Linear regression analysis of all cases indicated that spine density was not associated with neuritic plaque score but did display negative correlation with Braak staging.
Why it matters
This study compared dendritic spines in the prefrontal cortex of people who had Alzheimer's pathology with and without dementia. It found that spine density was reduced in those with dementia, suggesting structural features may relate to cognitive resilience, but it is a small post-mortem study and does not test a treatment or cure.
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Study details
- Evidence strengthLow
How this study scored 48/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Annals of neurology) |
| Journal's citation record | 3 / 4 | Annals of Neurology: journal h-index 437 (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 | 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 | 5 / 7 | Cited 204 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 18.5 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 4 / 6 | Cited 10.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 6 other studies in this library |
| Still being cited | 3 / 4 | Cited 65 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Jeremy H. Herskowitz: h-index 22 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Emory University: institution h-index 1,360 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28921611) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 48 / 100 | — |
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