Evidence map›Paper›PMID 41736303›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026

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 read
PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.
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.
Wenzhen DuanDivision of Neurobiology, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Hanzhang LuRussell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Zhiliang WeiRussell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/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 AG081932NIA NIH HHS R01AG081932NIBIB NIH HHS P41 EB031771NIBIB NIH HHS P41EB031771
6 · The paper itself

Abstract

introductionCerebrovascular reactivity (CVR) impairment is a key feature of Alzheimer's disease and related dementias (ADRD), 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 magnetic resonance imaging (MRI), including phase-contrast and pseudo-continuous arterial spin labeling, was performed in mouse models of amyloidosis (five familial Alzheimer's disease mutations [5xFAD]), VSMC degeneration (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL]), and lipopolysaccharide-induced neuroinflammation. Characterizations of vascular, amyloid beta, 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 beta 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 ADRD.

Indexed as

Alzheimer DiseaseCerebrovascular CirculationMuscle, Smooth, VascularMyocytes, Smooth MuscleNeuroinflammatory DiseasesAmyloid beta-PeptidesAnimalsBrainCADASILDisease Models, AnimalHumansInflammationMagnetic Resonance ImagingMaleMiceMice, TransgenicAmyloid beta-Peptidesalpha‐smooth muscle actinAlzheimer's diseasecerebral amyloid angiopathycerebral blood flowcerebrovascular reactivityneuroinflammationvascular smooth muscle cell

Identifiers

PMID41736303
PMCPMC12932915

What OpenQuestion holds

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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.