Potentiality of Graphene-Based Materials for Neural Repair

New treatments that can facilitate neural repair and reduce persistent impairments have significant value in promoting recovery following stroke. One technique that has gained interest is transcranial direct current stimulation (tDCS) as early research suggested it could enhance plasticity and enable greater behavioral recovery. However, several studies have now identified substantial inter-subject variability in response to tDCS and clinical trials revealed insufficient evidence of treatment effectiveness. A possible explanation for the varied and negative findings is that the physiological model of stroke recovery that researchers have used to guide the application of tDCS based treatments in stroke is overly simplistic and does not account for stroke heterogeneity or known determinants that affect the tDCS response. Here, we propose that tDCS could have a more clearly beneficial role in enhancing stroke recovery if greater consideration is given to individualizing treatment. By critically reviewing the proposed mechanisms of tDCS, stroke physiology across the recovery continuum, and known determinants of tDCS response, we propose a new, theoretical, patient-tailored approach to delivering tDCS after stroke. The proposed model includes a step-by-step principled selection strategy for identifying optimal neuromodulation targets and outlines key areas for further investigation. Tailoring tDCS treatment to individual neuroanatomy and physiology is likely our best chance at producing robust and meaningful clinical benefit for people with stroke and would, therefore, accelerate opportunities for clinical translation.

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miR-615 Fine-Tunes Growth and Development and Has a Role in Cancer and in Neural Repair

Cells ◽

10.3390/cells9071566 ◽

2020 ◽

Vol 9 (7) ◽

pp. 1566 ◽

Cited By ~ 1

Author(s):

Marisol Godínez-Rubí ◽

Daniel Ortuño-Sahagún

Keyword(s):

Growth And Development ◽

Target Genes ◽

Noncoding Rnas ◽

Tumor Promoter ◽

Neural Repair ◽

Small Noncoding Rnas ◽

Physiological Processes ◽

And Migration ◽

Migration Of Cells ◽

Regulation Of Growth

MicroRNAs (miRNAs) are small noncoding RNAs that function as epigenetic modulators regulating almost any gene expression. Similarly, other noncoding RNAs, as well as epigenetic modifications, can regulate miRNAs. This reciprocal interaction forms a miRNA-epigenetic feedback loop, the deregulation of which affects physiological processes and contributes to a great diversity of diseases. In the present review, we focus on miR-615, a miRNA highly conserved across eutherian mammals. It is involved not only during embryogenesis in the regulation of growth and development, for instance during osteogenesis and angiogenesis, but also in the regulation of cell growth and the proliferation and migration of cells, acting as a tumor suppressor or tumor promoter. It therefore serves as a biomarker for several types of cancer, and recently has also been found to be involved in reparative processes and neural repair. In addition, we present the pleiad of functions in which miR-615 is involved, as well as their multiple target genes and the multiple regulatory molecules involved in its own expression. We do this by introducing in a comprehensible way the reported knowledge of their actions and interactions and proposing an integral view of its regulatory mechanisms.

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Axon Regeneration in the Mammalian Optic Nerve

Annual Review of Vision Science ◽

10.1146/annurev-vision-022720-094953 ◽

2020 ◽

Vol 6 (1) ◽

pp. 195-213

Author(s):

Philip R. Williams ◽

Larry I. Benowitz ◽

Jeffrey L. Goldberg ◽

Zhigang He

Keyword(s):

Optic Nerve ◽

Ganglion Cells ◽

Traumatic Injury ◽

Optic Glioma ◽

Retinal Ganglion ◽

Degenerative Diseases ◽

Nerve Crush ◽

Neural Repair ◽

Molecular Logic ◽

Injury Models

The damage or loss of retinal ganglion cells (RGCs) and their axons accounts for the visual functional defects observed after traumatic injury, in degenerative diseases such as glaucoma, or in compressive optic neuropathies such as from optic glioma. By using optic nerve crush injury models, recent studies have revealed the cellular and molecular logic behind the regenerative failure of injured RGC axons in adult mammals and suggested several strategies with translational potential. This review summarizes these findings and discusses challenges for developing clinically applicable neural repair strategies.

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