Mouse Models of Stroke and Cerebral Small Vessel Disease in the MICRON Literature
About the MICRON Research Literature
These research pages organize published studies using MICRON imaging systems by animal species and the disease or condition investigated.
All publication counts and figures reflect the complete indexed research collection.
Explore related studies through the MICRON Research Hubs or search the complete publication collection in the reSEARCH portal.
Understanding Stroke and Cerebral Small Vessel Disease
Stroke is an acute focal neurological deficit produced by infarction or hemorrhage in central nervous system tissue. Cerebral small vessel disease is a chronic disorder of the brain's small perforating arteries, arterioles, capillaries and venules that presents as:
- Lacunar infarction
- White matter change
- Microbleeds
- Progressive cognitive impairment
The two are treated together because small vessel disease underlies a substantial share of lacunar ischemic events and of spontaneous intracerebral hemorrhage.
The retina is imaged alongside them because it develops as an outgrowth of the diencephalon and carries a microvasculature of comparable caliber behind a barrier of comparable construction to the blood-brain barrier, which makes small central nervous system vessels visible in a living subject in a way that cerebral vessels of the same size are not. Retinal vessel caliber, tortuosity and barrier leakage are studied in people on that basis.
Stroke and Cerebral Small Vessel Disease in Experimental Research
Two kinds of model recur in this literature, and what a retinal measurement means differs between them.
Where a cerebral artery is occluded experimentally the lesion sits in the brain and the retina is a separate tissue in which a change may or may not follow, so whether a retinal measurement there indexes the cerebral injury is contested rather than settled, and the two readings entail different things:
- If the retinal change does track the brain lesion, the retina supplies a remote readout of an injury sited elsewhere
- If it does not, the same measurement still describes how the occlusion affects a second central nervous system tissue, but cannot be read back as a statement about the brain
Deciding between those readings requires retinal and cerebral measurements made in the same animals and compared, which a retinal readout on its own cannot do.
In genetic models of monogenic small vessel disease, such as Notch3 and collagen IV mutant lines, the causative defect is expressed in the retinal and cerebral vascular beds at once, so the retina is affected tissue rather than a proxy for tissue injured elsewhere. What these models supply is the vascular lesion itself, its genetic cause where the model is genetic, its time course, and its response to intervention, followed repeatedly in the same living eye.
The parallel stops where the anatomy diverges: retinal ganglion cell axons are unmyelinated within the retina, so the white matter lesions that are among the defining imaging findings of human small vessel disease have no retinal counterpart, and the retina has neither a deep perforator territory nor the leptomeningeal collateral supply that shapes the extent of a cerebral infarct. Sporadic human small vessel disease also accumulates over decades against aging and hypertension that a rodent lifespan does not reproduce. Human cognitive and gait outcomes are not reproduced directly in an animal; model analogues require behavioral, learning, locomotor and gait assays whose relationship to patient-level clinical impairment has to be established rather than assumed. Some of the human retinal measurements used in this field are made in the macular capillary plexuses, which a mouse retina does not have.
Mouse Models of Stroke and Cerebral Small Vessel Disease
The mouse carries most of this work.
Transgenic and knockout lines allow a pathway to be removed or overexpressed, and cost, availability, short generation time and a large body of background data reinforce the choice.
A genetic manipulation constrains rather than isolates a mechanism: developmental compensation and pleiotropy remain possible.
Published MICRON Research: Stroke and Cerebral Small Vessel Disease in Mice
This page lists 4 papers from the MICRON literature, published 2015 to 2025, that study stroke or cerebral small vessel disease in mice.
Of these publications:
- 4 studies used mice as the primary stroke or cerebral small vessel disease disease model.
Scope of the literature collection: Publication counts reflect studies identified and indexed in the MICRON research corpus. This collection is not intended to represent an exhaustive review of all published stroke or cerebral small vessel disease research.
Which imaging and experimental techniques are used in these studies?
| Technique | Papers |
|---|---|
| Fundus Fluorescein Angiography | 2 |
Technique counts are paper-level co-occurrences and do not necessarily indicate that a technique was applied to the focal species or focal disease model.
Capabilities and Limitations of Imaging Techniques
A summary of what each imaging technique listed above can measure, the information it provides, and its limitations in research applications.
Fundus Fluorescein Angiography
Fundus fluorescein angiography uses an injected fluorescent dye to visualize blood flow through the retinal and choroidal circulation. Sequential images show how vessels fill, identify areas of reduced or absent perfusion, and reveal dye leakage associated with vascular abnormalities.
This technique is particularly useful for evaluating vascular perfusion, blood-retinal barrier integrity, and abnormal vessel growth. Fluorescein angiography primarily shows dye distribution rather than the surrounding retinal tissue. It provides a two-dimensional (en face) view in which vessels at different depths may overlap. Cross-sectional and cellular structural details require other imaging methods, such as optical coherence tomography (OCT) or optical coherence tomography angiography (OCT-A). Vascular abnormalities that do not affect dye filling or produce leakage may also remain undetected.
Which MICRON systems and add-ons appear?
| Instrument | Papers |
|---|---|
| MICRON III | 4 |
| Image-Guided Laser | 1 |
Which strains and genetic lines are used?
| Strain | Papers | Reported as |
|---|---|---|
| C57BL/6J | 2 | |
| C57BL/6 | 1 |
What other conditions are recorded on the same papers?
| Disease | Papers |
|---|---|
| Choroidal Neovascularization | 1 |
| Retinal Vein Occlusion (RVO) | 1 |
Which MICRON configurations appear in this work?
Configurations recorded in these papers, and the techniques recorded alongside them.
| MICRON configuration | Papers | Most frequent techniques recorded alongside |
|---|---|---|
| MICRON III | 4 | Fundus Fluorescein Angiography (2) |
| Image-Guided Laser | 1 |
The papers
| Year | Title | Journal | Role of focal species | MICRON products | Links |
|---|---|---|---|---|---|
| 2025 | Occludin acts as a dynein adaptor regulating permeability and collateral angiogenesis. | Proceedings of the National Academy of Sciences of the United States of America | Disease model | Image-Guided Laser, MICRON III | DOI · reSEARCH |
| 2017 | Therapeutic antibody targeting of Notch3 signaling prevents mural cell loss in CADASIL. | The Journal of Experimental Medicine | Disease model | MICRON III | DOI · reSEARCH |
| 2016 | Early retinal inflammatory biomarkers in the middle cerebral artery occlusion model of ischemic stroke. | Molecular Vision | Disease model | MICRON III | reSEARCH |
| 2015 | Molecular and Genetic Analyses of Collagen Type IV Mutant Mouse Models of Spontaneous Intracerebral Hemorrhage Identify Mechanisms for Stroke Prevention. | Circulation | Disease model | MICRON III | DOI · reSEARCH |
Browse all hubs at MICRON Research Hubs. The full corpus is searchable in the reSEARCH portal.