Related Experiment Video
Updated: Jun 8, 2026
Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
Published on: March 22, 2016
Anamnestic recall of stroke-related deficits: an animal model
Dannielle Zierath1, Jessica Hadwin, Anna Savos
1Department of Neurology, University of Washington School of Medicine, Harborview Medical Center, Seattle, WA, USA.
Background And Purpose:
Anamnestic recall of stroke-related deficits is a common clinical observation, especially during periods of systemic infection. The pathophysiology of this transient re-emergence of neurological dysfunction is unknown.
Methods:
Male Lewis rats underwent 3 hours middle cerebral artery occlusion and were treated with lipopolysaccharide or saline at the time of reperfusion. The delayed-type hypersensitivity (DTH) response to myelin basic protein was examined 28 days after middle cerebral artery occlusion. Changes in behavioral outcomes were assessed after DTH testing and repeat administration of lipopolysaccharide or saline at 34 days. At the time of euthanasia (36 days), the immunologic response of splenocytes to myelin basic protein, neuron-specific enolase, and proteolipid protein was determined by enzyme-linked immunospot assay and the number of lymphocytes in the brain determined by immunocytochemistry.
Results:
Animals treated with lipopolysaccharide at middle cerebral artery occlusion had a greater DTH response to myelin basic protein than animals treated with saline. Among those animals that had fully recovered on a given behavioral test before DTH testing, those treated with lipopolysaccharide at middle cerebral artery occlusion displayed more neurological deterioration after DTH testing and had more CD8(+) lymphocytes within the ischemic core of the brain. Furthermore, the Th1 immune response to brain antigens in the spleen was more robust among those animals that deteriorated after DTH testing and there were more CD4(+) lymphocytes in the penumbral region of animals with a Th1 response to myelin basic protein.
Conclusions:
Our data suggest that an immune response to the brain contributes to the phenomenon of anamnestic recall of stroke-related deficits after an infection. The contribution of the immune response to this phenomenon deserves further investigation.
Insights
Systemic infection can trigger stroke symptom recurrence. This study in rats suggests an immune response to brain antigens contributes to this anamnestic recall of stroke deficits, warranting further investigation.
Area of Science:
- Neuroscience
- Immunology
- Stroke Research
Background:
- Anamnestic recall of stroke deficits during infection is observed but poorly understood.
- The underlying pathophysiology of transient neurological dysfunction re-emergence remains unknown.
Purpose of the Study:
- To investigate the role of immune response in the anamnestic recall of stroke-related deficits.
- To explore the link between systemic infection and the exacerbation of neurological deficits post-stroke.
Main Methods:
- Male Lewis rats underwent middle cerebral artery occlusion (MCAO) and were treated with lipopolysaccharide (LPS) or saline.
- Delayed-type hypersensitivity (DTH) response to myelin basic protein was assessed.
- Behavioral outcomes, splenocyte immune response to brain antigens, and brain lymphocyte infiltration were analyzed.
Main Results:
- LPS treatment post-MCAO increased DTH response to myelin basic protein.
- Animals with LPS treatment showed greater neurological deterioration after DTH testing.
- Increased CD8+ lymphocytes in the ischemic core and enhanced Th1 immune response to brain antigens were observed in deteriorating animals.
Conclusions:
- Immune responses to brain antigens contribute to anamnestic recall of stroke deficits following infection.
- Further research is needed to elucidate the immune mechanisms involved in this phenomenon.
