Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (720 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Mechanism by which changes in neural activity are tightly associated with regional cortical hemodynamics and metabolism changes. The association is often inferred from neuroimaging signals (e.g., fMRI; or nir spectroscopy).
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Coupling, Neurovascular; Couplings, Neurovascular; Neurovascular Couplings; Cortical Hemodynamic Responses; Hemodynamic Response, Cortical; Hemodynamic Responses, Cortical; Response, Cortical Hemodynamic; Responses, Cortical Hemodynamic.
Where it fits in the MeSH classification
- Broader topics
- Cerebrovascular Circulation
- See also
- Hemodynamics
Related concepts
- Hemodynamics
- Neuroimaging
- Nir Spectroscopy
Research landscape
PubMed indexes 1,046 records tagged with the MeSH heading “Neurovascular Coupling” (counts retrieved 2026-10-29). 657 of them (62.8%) were published from 2020 onward, and the busiest period so far is 2020 onward with 657 records.
Reviews account for 226 records (21.6%) and meta-analyses for 3. Randomized controlled trials number 9 (0.9%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 0 |
| 2010-2019 | 413 |
| 2020 onward | 657 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 226 | 21.6% |
| Meta-analyses | 3 | 0.3% |
| Randomized controlled trials | 9 | 0.9% |
Method: PubMed query "Neurovascular Coupling"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Interaction of Microglia and Astrocytes in the Neurovascular Unit | 2020 | Review article Design not recorded in structured metadata | 460 | cc by PMID 32733433 · DOI · PMC7362712 |
| Microglia modulate blood flow, neurovascular coupling, and hypoperfusion via purinergic actions | 2022 | Research article Design not recorded in structured metadata | 228 | cc by PMID 35201268 · DOI · PMC8932534 |
| Validating a functional near-infrared spectroscopy diagnostic paradigm for Major Depressive Disorder | 2020 | Research article Design not recorded in structured metadata | 169 | cc by PMID 32546704 · DOI · PMC7298029 |
| BOLD signal changes can oppose oxygen metabolism across the human cortex | 2026 | Research article Design not recorded in structured metadata | 28 | cc by PMID 41402521 · DOI · PMC13156032 |
Interaction of Microglia and Astrocytes in the Neurovascular Unit [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The interaction between microglia and astrocytes significantly influences neuroinflammation.
- Closing excerpt
- Although both microglia and astrocytes have different functional characteristics, they can achieve immune "optimization" through their mutual communication and cooperation in the NVU and build a cascaded immune network of amplification.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (211 words)
The interaction between microglia and astrocytes significantly influences neuroinflammation. Microglia/astrocytes, part of the neurovascular unit (NVU), are activated by various brain insults. The local extracellular and intracellular signals determine their characteristics and switch of phenotypes. Microglia and astrocytes are activated into two polarization states: the pro-inflammatory phenotype (M1 and A1) and the anti-inflammatory phenotype (M2 and A2). During neuroinflammation, induced by stroke or lipopolysaccharides, microglia are more sensitive to pathogens, or damage; they are thus initially activated into the M1 phenotype and produce common inflammatory signals such as IL-1 and TNF-α to trigger reactive astrocytes into the A1 phenotype. These inflammatory signals can be amplified not only by the self-feedback loop of microglial activation but also by the unique anatomy structure of astrocytes. As the pathology further progresses, resulting in local environmental changes, M1-like microglia switch to the M2 phenotype, and M2 crosstalk with A2. While astrocytes communicate simultaneously with neurons and blood vessels to maintain the function of neurons and the blood-brain barrier (BBB), their subtle changes may be identified and responded by astrocytes, and possibly transferred to microglia. Although both microglia and astrocytes have different functional characteristics, they can achieve immune "optimization" through their mutual communication and cooperation in the NVU and build a cascaded immune network of amplification.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32733433 · DOI · PMC7362712
Microglia modulate blood flow, neurovascular coupling, and hypoperfusion via purinergic actions [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Microglia, the main immunocompetent cells of the brain, regulate neuronal function, but their contribution to cerebral blood flow (CBF) regulation has remained elusive.
- Closing excerpt
- Thus, our data reveal a previously unrecognized role for microglia in CBF regulation, with broad implications for common neurological diseases.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (166 words)
Microglia, the main immunocompetent cells of the brain, regulate neuronal function, but their contribution to cerebral blood flow (CBF) regulation has remained elusive. Here, we identify microglia as important modulators of CBF both under physiological conditions and during hypoperfusion. Microglia establish direct, dynamic purinergic contacts with cells in the neurovascular unit that shape CBF in both mice and humans. Surprisingly, the absence of microglia or blockade of microglial P2Y12 receptor (P2Y12R) substantially impairs neurovascular coupling in mice, which is reiterated by chemogenetically induced microglial dysfunction associated with impaired ATP sensitivity. Hypercapnia induces rapid microglial calcium changes, P2Y12R-mediated formation of perivascular phylopodia, and microglial adenosine production, while depletion of microglia reduces brain pH and impairs hypercapnia-induced vasodilation. Microglial actions modulate vascular cyclic GMP levels but are partially independent of nitric oxide. Finally, microglial dysfunction markedly impairs P2Y12R-mediated cerebrovascular adaptation to common carotid artery occlusion resulting in hypoperfusion. Thus, our data reveal a previously unrecognized role for microglia in CBF regulation, with broad implications for common neurological diseases.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35201268 · DOI · PMC8932534
Validating a functional near-infrared spectroscopy diagnostic paradigm for Major Depressive Disorder [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Reduced haemodynamic response in the frontotemporal cortices of patients with major depressive disorder (MDD) has been demonstrated using functional near-infrared spectroscopy (fNIRS).
- Closing excerpt
- Haemodynamic response measured by fNIRS during an English letter fluency task is a promising biomarker for MDD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (192 words)
Reduced haemodynamic response in the frontotemporal cortices of patients with major depressive disorder (MDD) has been demonstrated using functional near-infrared spectroscopy (fNIRS). Most notably, changes in cortical oxy-haemoglobin during a Japanese phonetic fluency task can differentiate psychiatric patients from healthy controls (HC). However, this paradigm has not been validated in the English language. Therefore, the present work aimed to distinguish patients with MDD from HCs, using haemodynamic response measured during an English letter fluency task. One hundred and five HCs and 105 patients with MDD took part in this study. NIRS signals during the verbal fluency task (VFT) was acquired using a 52-channel system, and changes in oxy-haemoglobin in the frontal and temporal regions were quantified. Depression severity, psychosocial functioning, pharmacotherapy and psychiatric history were noted. Patients with MDD had smaller changes in oxy-haemoglobin in the frontal and temporal cortices than HCs. In both regions of interest, oxy-haemoglobin was not associated with any of the clinical variables studied. 75.2% and 76.5% of patients with MDD were correctly classified using frontal and temporal region oxy-haemoglobin, respectively. Haemodynamic response measured by fNIRS during an English letter fluency task is a promising biomarker for MDD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32546704 · DOI · PMC7298029
BOLD signal changes can oppose oxygen metabolism across the human cortex [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Functional magnetic resonance imaging measures brain activity indirectly by monitoring changes in blood oxygenation levels, known as the blood-oxygenation-level-dependent (BOLD) signal, rather than directly measuring neuronal activity.
- Closing excerpt
- Our findings challenge the canonical interpretation of the BOLD signal, indicating that quantitative functional magnetic resonance imaging provides a more reliable assessment of both absolute and relative changes in neuronal activity.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (151 words)
Functional magnetic resonance imaging measures brain activity indirectly by monitoring changes in blood oxygenation levels, known as the blood-oxygenation-level-dependent (BOLD) signal, rather than directly measuring neuronal activity. This approach crucially relies on neurovascular coupling, the mechanism that links neuronal activity to changes in cerebral blood flow. However, it remains unclear whether this relationship is consistent for both positive and negative BOLD responses across the human cortex. Here we found that about 40% of voxels with significant BOLD signal changes during various tasks showed reversed oxygen metabolism, particularly in the default mode network. These 'discordant' voxels differed in baseline oxygen extraction fraction and regulated oxygen demand via oxygen extraction fraction changes, whereas 'concordant' voxels depended mainly on cerebral blood flow changes. Our findings challenge the canonical interpretation of the BOLD signal, indicating that quantitative functional magnetic resonance imaging provides a more reliable assessment of both absolute and relative changes in neuronal activity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41402521 · DOI · PMC13156032
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The Neurovascular Unit Coming of Age: A Journey through Neurovascular Coupling in Health and Disease [5]
- Research article Cerebral blood flow regulation and neurovascular dysfunction in Alzheimer disease [6]
- Research article Revisiting the neurovascular unit [7]
- Research article Neurovascular dysfunction and neurodegeneration in dementia and Alzheimer's disease [8]
- Research article Functional vascular contributions to cognitive impairment and dementia: mechanisms and consequences of cerebral autoregulatory dysfunction, endothelial impairment, and neurovascular uncoupling in aging [9]
- Research article Neurovascular and Cognitive Dysfunction in Hypertension [10]
References
- Liu LR, Liu JC, Bao JS, Bai QQ, Wang GQ. Interaction of Microglia and Astrocytes in the Neurovascular Unit. . 2020. PMID 32733433 · DOI · PMC7362712
- Császár E, Lénárt N, Cserép C, Környei Z, Fekete R, Pósfai B, et al.. Microglia modulate blood flow, neurovascular coupling, and hypoperfusion via purinergic actions. . 2022. PMID 35201268 · DOI · PMC8932534
- Husain SF, Yu R, Tang TB, Tam WW, Tran B, Quek TT, et al.. Validating a functional near-infrared spectroscopy diagnostic paradigm for Major Depressive Disorder. . 2020. PMID 32546704 · DOI · PMC7298029
- Epp SM, Castrillón G, Yuan B, Andrews-Hanna J, Preibisch C, Riedl V. BOLD signal changes can oppose oxygen metabolism across the human cortex. . 2026. PMID 41402521 · DOI · PMC13156032
- Iadecola C. The Neurovascular Unit Coming of Age: A Journey through Neurovascular Coupling in Health and Disease. Neuron. 2017. PMID 28957666 · DOI · PMC5657612
- Kisler K, Nelson AR, Montagne A, Zlokovic BV. Cerebral blood flow regulation and neurovascular dysfunction in Alzheimer disease. Nat Rev Neurosci. 2017. PMID 28515434 · DOI · PMC5759779
- Schaeffer S, Iadecola C. Revisiting the neurovascular unit. Nat Neurosci. 2021. PMID 34354283 · DOI · PMC9462551
- Nelson AR, Sweeney MD, Sagare AP, Zlokovic BV. Neurovascular dysfunction and neurodegeneration in dementia and Alzheimer's disease. Biochim Biophys Acta. 2016. PMID 26705676 · DOI · PMC4821735
- Toth P, Tarantini S, Csiszar A, Ungvari Z. Functional vascular contributions to cognitive impairment and dementia: mechanisms and consequences of cerebral autoregulatory dysfunction, endothelial impairment, and neurovascular uncoupling in aging. Am J Physiol Heart Circ Physiol. 2017. PMID 27793855 · DOI · PMC5283909
- Iadecola C, Gottesman RF. Neurovascular and Cognitive Dysfunction in Hypertension. Circ Res. 2019. PMID 30920929 · DOI · PMC6527115
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.