Evidence map›Paper›PMID 42682443›Full record

ArticleFrontiers in immunology2026

An analysis of cerebral amyloid angiopathy based on samples from human brain bank.

Yizhou Zhang, Mengyao Ye, Shixiong Mi, Yi Zhou, Qihan Yu, Jiayi Liang, Shiyi Wang, Qian Yang, Yuhong Su, Huixian Cui and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Yizhou Zhang *Department of Human Anatomy, Human Brain Bank, Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei Medical University, Shijiazhuang, China.
Mengyao Ye *Department of Human Anatomy, Human Brain Bank, Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei Medical University, Shijiazhuang, China.
Shixiong MiDepartment of Human Anatomy, Human Brain Bank, Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei Medical University, Shijiazhuang, China.
Yi ZhouDepartment of Human Anatomy, Human Brain Bank, Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei Medical University, Shijiazhuang, China.
Qihan YuDepartment of Human Anatomy, Human Brain Bank, Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei Medical University, Shijiazhuang, China.
Jiayi LiangDepartment of Neurology, The First Hospital of Hebei Medical University, Shijiazhuang, China.
Shiyi WangDepartment of Human Anatomy, Human Brain Bank, Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei Medical University, Shijiazhuang, China.
Qian YangDepartment of Human Anatomy, Human Brain Bank, Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei Medical University, Shijiazhuang, China.
Yuhong SuDepartment of Human Anatomy, Human Brain Bank, Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei Medical University, Shijiazhuang, China.
Huixian CuiDepartment of Human Anatomy, Human Brain Bank, Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei Medical University, Shijiazhuang, China.
Xiaowei MaDepartment of Neurology, The First Hospital of Hebei Medical University, Shijiazhuang, China.
Juan DuDepartment of Human Anatomy, Human Brain Bank, Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei Medical University, Shijiazhuang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Cerebral amyloid angiopathy (CAA) is a common age-associated cerebrovascular disease marked by amyloid-β (Aβ) accumulation in cerebral vessel walls, and it is tightly linked to Alzheimer's disease (AD) and cognitive impairment. However, the specific mechanism in CAA progression remains poorly elucidated. Methods: We analyzed 49 autopsy samples obtained from the Human Brain Bank of Hebei Medical University, collected basic pathological data and explored the correlations between CAA and Alzheimer's disease neuropathologic change (ADNC). Transcriptomic sequencing was performed on 21 occipital lobe specimens to screen differentially expressed genes underlying CAA and its pathological subtypes. Results: Neuropathological examination identified CAA pathology in 29 of 49 community donors (59.18%). Both CAA type and stage were significantly correlated with ADNC. In particular, CAA type 1 was closely associated with AD pathology and cognitive decline. Transcriptome analysis revealed that the GO functional enrichment was mainly concentrated in immune response-activating and -regulating signaling pathways. Triggering receptor expressed on myeloid cells 1 ( Conclusion: CAA is not simply an independent cerebrovascular disorder but also serves as a critical synergistic risk factor for ADNC progression.

Indexed as

BrainCerebral Amyloid AngiopathyAgedAged, 80 and overAlzheimer DiseaseAutopsyFemaleGene Expression ProfilingHumansMaleTissue BanksTranscriptomeAlzheimer’s disease neuropathologic changecerebral amyloid angiopathyhuman brain bankmicrogliaTREM1

Identifiers

PMID42682443
PMCPMC13529461

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.