Jonathan Edwards
"Gibberish"
- Messages
- 5,256
No idea if this is relevant to ME but it has some interestingly familiar bits in it.
J Neurosci. 2015 Feb 4;35(5):2133-45. doi: 10.1523/JNEUROSCI.4098-14.2015.
B-lymphocyte-mediated delayed cognitive impairment following stroke.
Doyle KP1, Quach LN2, Solé M3, Axtell RC2, Nguyen TV1, Soler-Llavina GJ4, Jurado S4, Han J2, Steinman L2, Longo FM2, Schneider JA5, Malenka RC4,Buckwalter MS6.
Abstract
Each year, 10 million people worldwide survive the neurologic injury associated with a stroke. Importantly, stroke survivors have more than twice the risk of subsequently developing dementia compared with people who have never had a stroke. The link between stroke and the later development of dementia is not understood. There are reports of oligoclonal bands in the CSF of stroke patients, suggesting that in some people a B-lymphocyte response to stroke may occur in the CNS. Therefore, we tested the hypothesis that a B-lymphocyte response to stroke could contribute to the onset of dementia. We discovered that, in mouse models, activated B-lymphocytes infiltrate infarcted tissue in the weeks after stroke. B-lymphocytesundergo isotype switching, and IgM, IgG, and IgA antibodies are found in the neuropil adjacent to the lesion. Concurrently, mice develop delayed deficits in LTP and cognition. Genetic deficiency, and the pharmacologic ablation of B-lymphocytes using an anti-CD20 antibody, prevents the appearance of delayed cognitive deficits. Furthermore, immunostaining of human postmortem tissue revealed that a B-lymphocyte response to stroke also occurs in the brain of some people with stroke and dementia. These data suggest that some stroke patients may develop a B-lymphocyte response to stroke that contributes to dementia, and is potentially treatable with FDA-approved drugs that target B cells.
J Neurosci. 2015 Feb 4;35(5):2133-45. doi: 10.1523/JNEUROSCI.4098-14.2015.
B-lymphocyte-mediated delayed cognitive impairment following stroke.
Doyle KP1, Quach LN2, Solé M3, Axtell RC2, Nguyen TV1, Soler-Llavina GJ4, Jurado S4, Han J2, Steinman L2, Longo FM2, Schneider JA5, Malenka RC4,Buckwalter MS6.
Abstract
Each year, 10 million people worldwide survive the neurologic injury associated with a stroke. Importantly, stroke survivors have more than twice the risk of subsequently developing dementia compared with people who have never had a stroke. The link between stroke and the later development of dementia is not understood. There are reports of oligoclonal bands in the CSF of stroke patients, suggesting that in some people a B-lymphocyte response to stroke may occur in the CNS. Therefore, we tested the hypothesis that a B-lymphocyte response to stroke could contribute to the onset of dementia. We discovered that, in mouse models, activated B-lymphocytes infiltrate infarcted tissue in the weeks after stroke. B-lymphocytesundergo isotype switching, and IgM, IgG, and IgA antibodies are found in the neuropil adjacent to the lesion. Concurrently, mice develop delayed deficits in LTP and cognition. Genetic deficiency, and the pharmacologic ablation of B-lymphocytes using an anti-CD20 antibody, prevents the appearance of delayed cognitive deficits. Furthermore, immunostaining of human postmortem tissue revealed that a B-lymphocyte response to stroke also occurs in the brain of some people with stroke and dementia. These data suggest that some stroke patients may develop a B-lymphocyte response to stroke that contributes to dementia, and is potentially treatable with FDA-approved drugs that target B cells.
