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32/100

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Brain tissue and pathology

Topic: Brain proteins, microglia and lab models

Plain-language summary

Cystatin C (CST3) colocalizes with amyloid-β (Aβ) around vessels in cerebral amyloid angiopathy (CAA). This study aimed to characterize CST3-Aβ interactions in CAA. Brain tissues from 12 Alzheimer disease (AD) and 5 non-AD control subjects, along with AD model mice (J20), were examined. In AD brains, immunohistochemistry revealed Aβ positivity around cortical and leptomeningeal vessels as well as in intra- and extracellular areas. Congo red-positive vessels were also present. Conversely, control brains showed only few Aβ-positive cells. CST3 was primarily intracellular in controls, but in AD, it was found both to be intracellular and perivascular, colocalizing with Aβ and Congo red in affected vessels. Vessel quantification showed a positive correlation between CST3-positive and Aβ- or Congo red-positive vessels. Moreover, most CST3-positive vessels were Cathepsin B (CatB)-negative. CatB was significantly decreased in AD and inversely correlated with CAA severity. Immunoprecipitation followed by Western blotting, dot blot, and TEM revealed oligomeric aggregates and short fibrillar CST3 bound to Aβ in both AD and J20 mice brains. In J20 mice, CST3 was only neuron-positive at 2 months, and vessel-positive, colocalizing with Aβ from 3 months. These findings suggest that aggregated CST3 binds to Aβ and accumulates around vessels, potentially contributing to CAA pathogenesis.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Bhuiya, J., Shibly, A. Z., Sheikh, A. M., Tabassum, S., Abdullah, F. B., Fahmida, J., et al. (2025). Deposition of aggregated cystatin C-amyloid-β complexes and reduced cathepsin B activity modulate cerebral amyloid angiopathy pathogenesis. Journal of Neuropathology & Experimental Neurology. https://doi.org/10.1093/jnen/nlaf138

Vancouver

Bhuiya J, Shibly AZ, Sheikh AM, Tabassum S, Abdullah FB, Fahmida J, et al. Deposition of aggregated cystatin C-amyloid-β complexes and reduced cathepsin B activity modulate cerebral amyloid angiopathy pathogenesis. Journal of Neuropathology & Experimental Neurology. 2025. doi:10.1093/jnen/nlaf138. PMID: 41411185.

BibTeX

@article{bhuiya2025-41411185,
  author  = {Bhuiya, Jubo and Shibly, Abu Zaffar and Sheikh, Abdullah Md. and Tabassum, Shatera and Abdullah, Fatema Binte and Fahmida, Jerin and Tamegai, Hiro and Aritake, Shun and others},
  title   = {{Deposition of aggregated cystatin C-amyloid-β complexes and reduced cathepsin B activity modulate cerebral amyloid angiopathy pathogenesis}},
  journal = {Journal of Neuropathology \& Experimental Neurology},
  year    = {2025},
  doi     = {10.1093/jnen/nlaf138},
  pmid    = {41411185},
  url     = {https://doi.org/10.1093/jnen/nlaf138}
}

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How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
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Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

In AD brains, immunohistochemistry revealed Aβ positivity around cortical and leptomeningeal vessels as well as in intra- and extracellular areas.
CatB was significantly decreased in AD and inversely correlated with CAA severity.
Immunoprecipitation followed by Western blotting, dot blot, and TEM revealed oligomeric aggregates and short fibrillar CST3 bound to Aβ in both AD and J20 mice brains.
These findings suggest that aggregated CST3 binds to Aβ and accumulates around vessels, potentially contributing to CAA pathogenesis.

Why it matters

Examining brain tissue from 12 Alzheimer disease and 5 control subjects plus AD model mice, this study found that aggregated cystatin C binds to amyloid-β and accumulates around vessels, and that cathepsin B was significantly decreased in AD and inversely correlated with CAA severity. These findings suggest a possible contribution to CAA pathogenesis but no treatment, cure or prevention is tested.

Study details

Evidence strengthLow

How this study scored 32/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of Neuropathology & Experimental Neurology)
Journal's citation record	2 / 4	Journal of Neuropathology & Experimental Neurology: journal h-index 239 (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	4 / 5	2025 — within 3 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)
Randomized / blinded	0 / 2	No randomization 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	0.3 citations a year over 3 year(s) since 2025
Impact for its field and year	1 / 6	Cited 0.5× 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	3 / 4	Last-listed author Atsushi Nagai: h-index 66 (OpenAlex, whole career)
Institution's track record	0 / 3	Shimane University: institution h-index 241 (OpenAlex)
Multicenter collaboration	1 / 3	OpenAlex lists 2 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 41411185)
Free to read	0 / 2	Behind a paywall — scores zero
Total	32 / 100	—

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