Photobiomodulation therapy promotes neurogenesis by improving post-stroke local microenvironment and stimulating neuroprogenitor cells

Sounds promising. You will have to have your doctor contact their stroke research partners to get this tested in humans. If they don't have partners your stroke department head is incompetent along with your stroke hospital president.  With no partners they are just inert and useless doctors,

WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM?

I could see significant problems getting through the skull to actually affect the brain itself. But that is for your doctor and researchers to solve.
http://www.sciencedirect.com/science/article/pii/S001448861730273X 

Author links open overlay panelLuodanYang^abDonovanTucker^bYanDong^bChongyunWu^aYujiaoLu^bYongLi^bJuanZhang^bTimon Cheng-YiLiu^aQuanguangZhang;

https://doi.org/10.1016/j.expneurol.2017.10.013Get rights and content

Highlights

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PBM alleviates behavioral deficits after PT stroke.

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PBM decreases cortical infarct size and increases neuronal survival.

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PBM promotes cortical neurogenesis after PT stroke.

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PBM inhibits local inflammatory status and promotes mitochondrial function.

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PBM promotes proliferation and differentiation of neuroprogenitor cells.

Abstract

Recent work has indicated that photobiomodulation (PBM), also known as low-level laser/light therapy (LLLT), may beneficially alter the pathological status of several neurological disorders, although the mechanism currently remains unclear. The current study was designed to investigate the beneficial effect of PBM on behavioral deficits and neurogenesis in a photothrombotic (PT) model of ischemic stroke in rats. From day 1 to day 7 after the establishment of PT model, 2-minute daily PBM (CW, 808 nm, 350 mW/cm², total 294 J at scalp level) was applied on the infarct injury area (1.8 mm anterior to the bregma and 2.5 mm lateral from the midline). Rats received intraperitoneal injections of 5-bromodeoxyuridine (BrdU) twice daily (50 mg/kg) from day 2 to 8 post-stoke, and samples were collected at day 14. We demonstrated that PBM significantly attenuated behavioral deficits and infarct volume induced by PT stroke. Further investigation displayed that PBM remarkably enhanced neurogenesis and synaptogenesis, as evidenced by immunostaining of BrdU, Ki67, DCX, MAP2, spinophilin, and synaptophysin. Mechanistic studies suggested beneficial effects of PBM were accompanied by robust suppression of reactive gliosis and the production of pro-inflammatory cytokines. On the contrary, the release of anti-inflammatory cytokines, cytochrome c oxidase activity and ATP production in peri-infarct regions were elevated following PBM treatment. Intriguingly, PBM could effectively switch an M1 microglial phenotype to an anti-inflammatory M2 phenotype. Our novel findings indicated that PBM is capable of promoting neurogenesis after ischemic stroke. The underlying mechanisms may rely on: 1) promotion of proliferation and differentiation of internal neuroprogenitor cells in the peri-infarct zone; 2) improvement of the neuronal microenvironment by altering inflammatory status and promoting mitochondrial function. These findings provide strong support for the promising therapeutic effect of PBM on neuronal repair following ischemic stroke.