Deans' stroke musings: B-Lymphocyte-Mediated Delayed Cognitive Impairment following Stroke

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, July 30, 2015

B-Lymphocyte-Mediated Delayed Cognitive Impairment following Stroke

With double the risk of dementia post-stroke your doctor better have a protocol to prevent that. But I bet s/he does not have anything at all. You're screwed.
http://www.jneurosci.org/content/35/5/2133.abstract?

Kristian P. Doyle¹,²,
Lisa N. Quach¹,
Montse Solé¹,³,
Robert C. Axtell¹,
Thuy-Vi V. Nguyen¹,²,
Gilberto J. Soler-Llavina⁴,
Sandra Jurado⁴,
Jullet Han¹,
Lawrence Steinman¹,
Frank M. Longo¹,
Julie A. Schneider⁵,
Robert C. Malenka⁴, and
Marion S. Buckwalter¹,⁶

+Show Affiliations

Author contributions: K.P.D., L.N.Q., M.S., R.C.A., T.V.V.N., GJ..S.-L., S.J., J.H., L.S., F.M.L., J.A.S., R.C.M., and M.S.B. designed research; K.P.D., L.N.Q., M.S., R.C.A., T.V.V.N., G.J.S.-L., S.J., and J.H. performed research; J.A.S. contributed unpublished reagents/analytic tools; K.P.D., R.C.M., and M.S.B. analyzed data; K.P.D., J.A.S., and M.S.B. wrote the paper.

The Journal of Neuroscience, 4 February 2015, 35(5): 2133-2145; doi: 10.1523/JNEUROSCI.4098-14.2015

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-lymphocytes undergo 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.