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Microglial reactivity predicts hippocampal, but not global, atrophy in cerebral small vessel disease
Adriana Zainurin, Robin B. Brown, Daniel J. Tozer, Hugh Stephen Markus. Alzheimer s & Dementia, 2026-04-01
Topic: Brain proteins, microglia and lab models
Abstract INTRODUCTION Cerebral small vessel disease (CSVD) is the most prevalent pathology underlying vascular dementia. Increased neuroinflammation and blood‐brain barrier (BBB) permeability have been implicated in CSVD pathogenesis. We determined whether microglial reactivity and BBB permeability at baseline predicted whole‐brain and hippocampal atrophy over one year, and cognitive impairment over four years. METHODS Seventy‐seven patients with CSVD were recruited to this prospective study. Baseline microglial reactivity and BBB permeability were determined using 11 C‐PK11195 positron emission tomography and dynamic contrast enhanced (DCE) MRI respectively. RESULTS Greater 11 C‐PK11195 binding at baseline was associated with hippocampal atrophy over one year ( p = 0.001), but not with global brain atrophy. Cox regression analyses showed no significant associations between 11 C‐PK11195 and cognitive impairment. There were no associations between BBB permeability with whole‐brain and hippocampal atrophy, or with cognitive impairment. DISCUSSION Our data suggests that microglial reactivity may play a role in hippocampal atrophy; potentially contributing to the increasingly recognized interaction between vascular and neurodegenerative pathology.
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APA 7th
Zainurin, A., Brown, R. B., Tozer, D. J., & Markus, H. S. (2026). Microglial reactivity predicts hippocampal, but not global, atrophy in cerebral small vessel disease. Alzheimer s & Dementia. https://doi.org/10.1002/alz.71336
Vancouver
Zainurin A, Brown RB, Tozer DJ, Markus HS. Microglial reactivity predicts hippocampal, but not global, atrophy in cerebral small vessel disease. Alzheimer s & Dementia. 2026. doi:10.1002/alz.71336. PMID: 41927515.
BibTeX
@article{zainurin2026-41927515,
author = {Zainurin, Adriana and Brown, Robin B. and Tozer, Daniel J. and Markus, Hugh Stephen},
title = {{Microglial reactivity predicts hippocampal, but not global, atrophy in cerebral small vessel disease}},
journal = {Alzheimer s \& Dementia},
year = {2026},
doi = {10.1002/alz.71336},
pmid = {41927515},
url = {https://doi.org/10.1002/alz.71336}
}
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Key findings
- RESULTS Greater 11 C‐PK11195 binding at baseline was associated with hippocampal atrophy over one year ( p = 0.001), but not with global brain atrophy.
- Cox regression analyses showed no significant associations between 11 C‐PK11195 and cognitive impairment.
- DISCUSSION Our data suggests that microglial reactivity may play a role in hippocampal atrophy; potentially contributing to the increasingly recognized interaction between vascular and neurodegenerative pathology.
Why it matters
In 77 patients with cerebral small vessel disease, greater baseline microglial reactivity was associated with hippocampal atrophy over one year but not with global brain atrophy, and there were no significant associations with cognitive impairment. Blood-brain barrier permeability was not associated with atrophy or cognitive impairment, and the authors suggest microglial reactivity may play a role in hippocampal atrophy.
Study details
- Evidence strengthLow
How this study scored 38/100
Published in a peer-reviewed 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 | 7 / 10 | Tier 3 — peer-reviewed journal (Alzheimer s & Dementia) |
| Journal's citation record | 2 / 4 | Alzheimer s & Dementia: journal h-index 228 (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 | 5 / 5 | 2026 — within 1 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 | 1 / 7 | Cited 1 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.5 citations a year over 2 year(s) since 2026 |
| Impact for its field and year | 2 / 6 | Cited 2.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 0 / 4 | Cited 1 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Hugh Stephen Markus: h-index 137 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Cambridge: institution h-index 1,973 (OpenAlex) |
| Multi-centre 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 41927515) |
| Free to read | 2 / 2 | Free to read |
| Total | 38 / 100 | — |
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