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.

Saturday, December 21, 2019

Early Stroke Induces Long-Term Impairment of Adult Neurogenesis Accompanied by Hippocampal-Mediated Cognitive Decline

There might be something here, but I don't know. 

Early Stroke Induces Long-Term Impairment of Adult Neurogenesis Accompanied by Hippocampal-Mediated Cognitive Decline

 Carolin Kathner-Schaffert 1, Lina Karapetow 1, Madlen Günther 1, Max Rudolph 1, Mahmoud Dahab 1, Eileen Baum 1, Thomas Lehmann 2, Otto W. Witte 1, Christoph Redecker 1, Christian W. Schmeer 1 and Silke Keiner 1,* 1 Hans-Berger Department of Neurology, Jena University Hospital, Am Klinikum 1, 07747 Jena, Germany; Carolin.Kathner-Schaffert@med.uni-jena.de (C.K.-S.); Lina.Karapetow@med.uni-jena.de (L.K.); Madlen.Guenther@med.uni-jena.de (M.G.); Max.Rudolph@uni-jena.de (M.R.); Mahmoud.Mohamed@med.uni-jena.de (M.D.); Eileen.Baum@noldus.com (E.B.); Otto.Witte@med.uni-jena.de (O.W.W.); Christoph.Redecker@klinikum-lippe.de (C.R.); Christian.Schmeer@med.uni-jena.de (C.W.S.) 2 Institute of Medical Statistics and Computer Science, University Hospital Jena, Friedrich Schiller University Jena, 07743 Jena, Germany; Thomas.Lehmann@med.uni-jena.de * Correspondence: silke.keiner@med.uni-jena.de; Tel.: +49-364-1932-5914
Received: 14 October 2019; Accepted: 12 December 2019; Published: 17 December 2019
 

Abstract: 


Stroke increases neurogenesis in the adult dentate gyrus in the short term, however, long-term effects at the cellular and functional level are poorly understood. Here we evaluated the impact of an early stroke lesion on neurogenesis and cognitive function of the aging brain. We hypothesized that a stroke disturbs dentate neurogenesis during aging correlate with impaired flexible learning. To address this issue a stroke was induced in 3-month-old C57Bl/6 mice by a middle cerebral artery occlusion (MCAO). To verify long-term changes of adult neurogenesis the thymidine analogue BrdU (5-Bromo-20-deoxyuridine) was administrated at different time points during aging. One and half months after BrdU injections learning and memory performance were assessed with a modified version of the Morris water maze (MWM) that includes the re-learning paradigm, as well as hippocampus-dependent and -independent search strategies. After MWM performance mice were transcardially perfused. To further evaluate in detail the stroke-mediated changes on stem- and progenitor cells as well as endogenous proliferation nestin-green-fluorescent protein (GFP) mice were used. Adult nestin-GFP mice received a retroviral vector injection in the hippocampus to evaluate changes in the neuronal morphology. At an age of 20 month the nestin-GFP mice were transcardially perfused after MWM performance and BrdU application 1.5 months later. The early stroke lesion significantly decreased neurogenesis in7.5-and 9-month-old animals and also endogenous proliferation in the latter group. Furthermore, immature double cortin (DCX)-positive neurons were reduced in 20-month-old nestin-GFP mice after lesion. All MCAO groups showed an impaired performance in the MWM and mostly relied on hippocampal independent search strategies. These findings indicate that an early ischemic insult leads to a dramatical decline of neurogenesis during aging that correlates with a premature development of hippocampal dependent deficits. Our study supports the notion that an early stroke might lead to long-term cognitive deficits as observed in human patients after lesion.

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