Involvement of calpains in adult neurogenesis: implications for stroke

What is your doctor doing with this to make a stroke protocol? Or is he/she one of the lazy ones? Waiting around for somebody else to solve the problem?
I don't give a shit that this is a hypothesis and theory article. That just means your doctor has to come up with a clinical research trial to test whatever theory they believe in.
I can almost guarantee that nothing will be done to follow up on this. We just do not have a great stroke association leading the strategy.
http://journal.frontiersin.org/article/10.3389/fncel.2015.00022/full?
Vanessa M. Machado^1,2,3,4, Maria I. Morte⁴, Bruno P. Carreira⁴, Maria M. Azevedo^4†, Jiro Takano⁵, Nobuhisa Iwata⁶, Takaomi C. Saido⁵, Hannelore Asmussen⁷, Alan R. Horwitz⁷, Caetana M. Carvalho⁴ and Inês M. Araújo^1,2,3,4*

• ¹Regenerative Medicine Program, Department of Biomedical Sciences and Medicine, University of Algarve, Faro, Portugal
• ²IBB-Institute for Biotechnology and Bioengineering, Center for Molecular and Structural Biomedicine, University of Algarve, Faro, Portugal
• ³Center for Biomedical Research, CBMR, University of Algarve, Faro, Portugal
• ⁴Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
• ⁵Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako-shi, Saitama, Japan
• ⁶Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan
• ⁷Department of Cell Biology, University of Virginia School of Medicine, Charlottesville, VA, USA

Calpains are ubiquitous proteases involved in cell proliferation, adhesion and motility. In the brain, calpains have been associated with neuronal damage in both acute and neurodegenerative disorders, but their physiological function in the nervous system remains elusive. During brain ischemia, there is a large increase in the levels of intracellular calcium, leading to the activation of calpains. Inhibition of these proteases has been shown to reduce neuronal death in a variety of stroke models. On the other hand, after stroke, neural stem cells (NSC) increase their proliferation and newly formed neuroblasts migrate towards the site of injury. However, the process of forming new neurons after injury is not efficient and finding ways to improve it may help with recovery after lesion. Understanding the role of calpains in the process of neurogenesis may therefore open a new window for the treatment of stroke. We investigated the involvement of calpains in NSC proliferation and neuroblast migration in two highly neurogenic regions in the mouse brain, the dentate gyrus (DG) and the subventricular zone (SVZ). We used mice that lack calpastatin, the endogenous calpain inhibitor, and calpains were also modulated directly, using calpeptin, a pharmacological calpain inhibitor. Calpastatin deletion impaired both NSC proliferation and neuroblast migration. Calpain inhibition increased NSC proliferation, migration speed and migration distance in cells from the SVZ. Overall, our work suggests that calpains are important for neurogenesis and encourages further research on their neurogenic role. Prospective therapies targeting calpain activity may improve the formation of new neurons following stroke, in addition to affording neuroprotection.