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B-lymphocyte-mediated delayed cognitive impairment following stroke
Kristian P Doyle1, Lisa N Quach2, Montse Solé3
1Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, Department of Immunobiology, Department of Neurology, and the Arizona Center on Aging, University of Arizona, Tucson, Arizona 85724.
Summary
Stroke survivors face increased dementia risk. A B-lymphocyte response in the brain after stroke may drive this dementia onset, offering potential therapeutic targets for stroke patients.
Area of Science:
- Neuroscience
- Immunology
Background:
- Stroke survivors have a significantly higher risk of developing dementia.
- The underlying mechanisms linking stroke to dementia remain unclear.
- Previous findings suggest a potential B-lymphocyte response in the central nervous system (CNS) following stroke.
Purpose of the Study:
- To investigate the hypothesis that a B-lymphocyte response to stroke contributes to dementia development.
- To explore the role of B-lymphocytes in the neurological and cognitive consequences of stroke.
Main Methods:
- Utilized mouse models of stroke to observe B-lymphocyte infiltration and activity in brain tissue.
- Administered anti-CD20 antibody to deplete B-lymphocytes in stroke models.
- Examined human postmortem brain tissue from stroke patients with and without dementia.
Main Results:
- Activated B-lymphocytes were found to infiltrate infarcted brain tissue in mice weeks after stroke.
- Mice lacking B-lymphocytes or treated with anti-CD20 antibody did not develop delayed cognitive deficits.
- Human postmortem analysis confirmed B-lymphocyte responses in the brains of some stroke patients with dementia.
Conclusions:
- A B-lymphocyte response to stroke occurs in both mouse models and human patients.
- This B-lymphocyte activity following stroke may contribute to the development of dementia.
- Targeting B-cells with existing therapies presents a potential treatment strategy for stroke-related dementia.
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