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.

Showing posts with label CXCL13. Show all posts
Showing posts with label CXCL13. Show all posts

Sunday, December 13, 2015

Lack of NG2 exacerbates neurological outcome and modulates glial responses after traumatic brain injury

The words counteract neurological deficits should produce an immediate response from our fucking failures of stroke associations to sponsor human research into this. But it won't, so you'll be screwed for at least another 50 years. No idea what NG 2 is, so ask your doctor.
http://onlinelibrary.wiley.com/doi/10.1002/glia.22944/abstract;jsessionid=8B564CA4B4BA2B2D7FFA3B1120DA65D6.f03t01?userIsAuthenticated=false&deniedAccessCustomisedMessage= 
 

  1. Changsheng Huang1,
  2. Dominik Sakry2,
  3. Lutz Menzel1,
  4. Larissa Dangel1,
  5. Anne Sebastiani1,
  6. Tobias Krämer1,
  7. Khalad Karram2,4,
  8. Kristin Engelhard1,3,
  9. Jacqueline Trotter2,3 and
  10. Michael K.E. Schäfer1,3,*
Article first published online: 6 DEC 2015
DOI: 10.1002/glia.22944
Article has an altmetric score of 10

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Keywords:

  • astrocytes;
  • microglia;
  • macrophages;
  • gliosis;
  • CNS inflammation;
  • Cxcl13
Traumatic brain injury (TBI) is a major cause of death and disability. The underlying pathophysiology is characterized by secondary processes including neuronal death and gliosis. To elucidate the role of the NG2 proteoglycan we investigated the response of NG2-knockout mice (NG2-KO) to TBI. Seven days after TBI behavioral analysis, brain damage volumetry and assessment of blood brain barrier integrity demonstrated an exacerbated response of NG2-KO compared to wild-type (WT) mice. Reactive astrocytes and expression of the reactive astrocyte and neurotoxicity marker Lcn2 (Lipocalin-2) were increased in the perilesional brain tissue of NG2-KO mice. In addition, microglia/macrophages with activated morphology were increased in number and mRNA expression of the M2 marker Arg1 (Arginase 1) was enhanced in NG2-KO mice. While TBI-induced expression of pro-inflammatory cytokine genes was unchanged between genotypes, PCR array screening revealed a marked TBI-induced up-regulation of the C-X-C motif chemokine 13 gene Cxcl13 in NG2-KO mice. CXCL13, known to attract immune cells to the inflamed brain, was expressed by activated perilesional microglia/macrophages seven days after TBI. Thirty days after TBI, NG2-KO mice still exhibited more pronounced neurological deficits than WT mice, up-regulation of Cxcl13, enhanced CD45+ leukocyte infiltration and a relative increase of activated Iba-1+/CD45+ microglia/macrophages. Our study demonstrates that lack of NG2 exacerbates the neurological outcome after TBI and associates with abnormal activation of astrocytes, microglia/macrophages and increased leukocyte recruitment to the injured brain. These findings suggest that NG2 may counteract neurological deficits and adverse glial responses in TBI. GLIA 2015
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Tuesday, August 25, 2015

Inflammation without neuronal death triggers striatal neurogenesis comparable to stroke

What is your doctor doing to mimic this in your stroke recovery? ANYTHING AT ALL?
Sounds like something useful for us.
Inflammation without neuronal death triggers striatal neurogenesis comparable to stroke
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doi:10.1016/j.nbd.2015.08.013
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Highlights

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LPS-induced inflammation without neuronal loss triggers striatal neurogenesis
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Magnitude of striatal neurogenesis is similar to that after stroke-induced injury
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Microarray on sorted microglia identifies factors potentially regulating neurogenesis
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CXCL13 is upregulated in microglia and increases neuroblast migration in vitro
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Microglia-derived CXCL13, acting through CXCR5, might be neuroprotective in stroke

Abstract

Ischemic stroke triggers neurogenesis from neural stem/progenitor cells (NSPCs) in the subventricular zone (SVZ) and migration of newly formed neuroblasts towards the damaged striatum where they differentiate to mature neurons. Whether it is the injury per se or the associated inflammation that gives rise to this endogenous neurogenic response is unknown. Here we showed that inflammation without corresponding neuronal loss caused by intrastriatal lipopolysaccharide (LPS) injection leads to striatal neurogenesis in rats comparable to that after a 30 min middle cerebral artery occlusion, as characterized by striatal DCX + neuroblast recruitment and mature NeuN +/BrdU + neuron formation. Using global gene expression analysis, changes in several factors that could potentially regulate striatal neurogenesis were identified in microglia sorted from SVZ and striatum of LPS-injected and stroke-subjected rats. Among the upregulated factors, one chemokine, CXCL13, was found to promote neuroblast migration from neonatal mouse SVZ explants in vitro. However, neuroblast migration to the striatum was not affected in constitutive CXCL13 receptor CXCR5−/− mice subjected to stroke. Infarct volume and pro-inflammatory M1 microglia/macrophage density were increased in CXCR5−/− mice, suggesting that microglia-derived CXCL13, acting through CXCR5, might be involved in neuroprotection following stroke. Our findings raise the possibility that the inflammation accompanying an ischemic insult is the major inducer of striatal neurogenesis after stroke.
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