Evidence map›Paper›PMID 41573926›Full record

ArticlebioRxiv : the preprint server for biology2025

Vascular smooth muscle cell loss, but not neuroinflammation, drives cerebrovascular reactivity impairment in Alzheimer's disease.

Xiuli Yang, Yuguo Li, Minmin Yao, Adnan Bibic, Wenzhen Duan, Hanzhang Lu, Zhiliang Wei

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. 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

5 · Who and what money

Authors and funding

7 authors.

Xiuli YangRussell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0001-8277-4285
Yuguo LiRussell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Minmin YaoDivision of Neurobiology, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Adnan BibicF. M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Research Institute, Baltimore, Maryland, USA.ORCID 0000-0001-8044-2906
Wenzhen DuanDivision of Neurobiology, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0001-5933-6308
Hanzhang LuRussell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0003-3871-1564
Zhiliang WeiRussell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-8477-2440

Funding

TRD 4: Platforms for multi-modal and multi-scale imaging dataP41EB031771 · NIBIB · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI Hanzhang Lu, Peter CM Van Zijl · 2021 to 2026
$9.9M
Pathophysiological mechanisms of hypoperfusion in mouse models of Alzheimer?s disease and small vessel diseaseR01AG081932 · NIA · JOHNS HOPKINS UNIVERSITY · PI Zhiliang Wei · 2023 to 2026
$2.1M
NIA NIH HHS R01 AG081932NIBIB NIH HHS P41 EB031771
6 · The paper itself

Abstract

introductionCerebrovascular reactivity (CVR) impairment is a key feature of Alzheimer's disease (AD), but its mechanistic basis remains unclear. This study examined whether vascular smooth muscle cell (VSMC) loss, rather than amyloidosis or neuroinflammation, underlies CVR deficits.

methodsNon-contrast MRI, including phase-contrast and pseudo-continuous arterial spin labeling, was performed in mouse models of amyloidosis (5xFAD), VSMC degeneration (CADASIL), and lipopolysaccharide-induced neuroinflammation. Characterization of vascular, amyloid-β, and inflammatory markers were performed for pathological assessment.

resultsCVR impairment emerged only when VSMC loss was present in CADASIL mice and at older ages in 5xFAD mice (9-12 months). Amyloid-β deposition occurred earlier than VSMC loss or CVR decline. Neuroinflammation primarily altered baseline cerebral blood flow without affecting CVR or VSMC integrity. DISCUSSION: These findings identify VSMC degeneration as an important driver of CVR impairment independent of cerebral amyloid angiopathy or inflammation, highlighting vascular integrity as a potential therapeutic target in AD.

Indexed as

alpha-smooth muscle actinAlzheimer’s diseasecerebral amyloid angiopathycerebral blood flowerebrovascular reactivityneuroinflammationvascular smooth muscle cell

Identifiers

PMID41573926
PMCPMC12822721

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Registered trials

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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.