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Bridging the Divide between Neuroprosthetic Design, Tissue Engineering and Neurobiology.

Leach JB, Achyuta AK, Murthy SK - Front Neuroeng (2010)

Bottom Line: Neuroprosthetic devices have made a major impact in the treatment of a variety of disorders such as paralysis and stroke.Within the context of the device-nervous system interface and central nervous system implants, areas of synergistic opportunity are discussed, including platforms to present cells with multiple cues, controlled delivery of bioactive factors, three-dimensional constructs and in vitro models of gliosis and brain injury, nerve regeneration strategies, and neural stem/progenitor cell biology.Finally, recent insights gained from the fields of developmental neurobiology and cancer biology are discussed as examples of exciting new biological knowledge that may provide fresh inspiration toward novel technologies to address the complexities associated with long-term neuroprosthetic device performance.

View Article: PubMed Central - PubMed

Affiliation: Department of Chemical and Biochemical Engineering, University of Maryland Baltimore, MD, USA.

ABSTRACT
Neuroprosthetic devices have made a major impact in the treatment of a variety of disorders such as paralysis and stroke. However, a major impediment in the advancement of this technology is the challenge of maintaining device performance during chronic implantation (months to years) due to complex intrinsic host responses such as gliosis or glial scarring. The objective of this review is to bring together research communities in neurobiology, tissue engineering, and neuroprosthetics to address the major obstacles encountered in the translation of neuroprosthetics technology into long-term clinical use. This article draws connections between specific challenges faced by current neuroprosthetics technology and recent advances in the areas of nerve tissue engineering and neurobiology. Within the context of the device-nervous system interface and central nervous system implants, areas of synergistic opportunity are discussed, including platforms to present cells with multiple cues, controlled delivery of bioactive factors, three-dimensional constructs and in vitro models of gliosis and brain injury, nerve regeneration strategies, and neural stem/progenitor cell biology. Finally, recent insights gained from the fields of developmental neurobiology and cancer biology are discussed as examples of exciting new biological knowledge that may provide fresh inspiration toward novel technologies to address the complexities associated with long-term neuroprosthetic device performance.

No MeSH data available.


Related in: MedlinePlus

Intensity of glial scarring in rats based on implantation procedure. (A,B) show co-expression analysis of GFAP (red) and vimentin (green) of implanted hollow fiber membranes (HFMs) in rats via two implantation schemes. Vimentin is expressed by astrocytes, microglia and fibroblasts derived from the meninges and other connective tissues. (A) Intraparenchymal implant (where the entire implant is surrounded by brain tissue) show less vimentin immunoreactivity along with GFAP reactivity. (B) Transcranial HFMs show thick layers of GFAP+/vimentin+ cells suggesting meningeal fibroblast infiltration due to skull-tethering of HFMs in such implants. The same study also showed higher ED1 reactivity in transcranial implants compared to intraparenchymal implants highlighting the exacerbated gliosis in the former implantation scheme. Scale = 100 μm. Reprinted from Kim et al. (2004). Copyright 2003, with permission from Elsevier.
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Figure 6: Intensity of glial scarring in rats based on implantation procedure. (A,B) show co-expression analysis of GFAP (red) and vimentin (green) of implanted hollow fiber membranes (HFMs) in rats via two implantation schemes. Vimentin is expressed by astrocytes, microglia and fibroblasts derived from the meninges and other connective tissues. (A) Intraparenchymal implant (where the entire implant is surrounded by brain tissue) show less vimentin immunoreactivity along with GFAP reactivity. (B) Transcranial HFMs show thick layers of GFAP+/vimentin+ cells suggesting meningeal fibroblast infiltration due to skull-tethering of HFMs in such implants. The same study also showed higher ED1 reactivity in transcranial implants compared to intraparenchymal implants highlighting the exacerbated gliosis in the former implantation scheme. Scale = 100 μm. Reprinted from Kim et al. (2004). Copyright 2003, with permission from Elsevier.

Mentions: The aforementioned events are restricted to the acute and chronic response of the brain tissue upon implanting a foreign object. However, other factors such as device insertion technique [manual (Stensaas and Stensaas, 1976; Liu et al., 1999) or robotic (Maynard et al., 2000; Csicsvari et al., 2003; Nicolelis et al., 2003; Szarowski et al., 2003)], speed of insertion (Edell et al., 1992; Nicolelis et al., 2003; Bjornsson et al., 2006), and most importantly, implantation approach (Biran et al., 2007) all have been reported to affect the biological response significantly. For instance, Kim et al. (2004) elegantly compared the biological response elicited by two implantation schemes in rat cortices (Figure 6). The first scheme utilized was transcranial implantation (a practical model with respect to neuroelectrodes) of hollow fiber membranes (HFMs) and the second scheme was intracranial implantation. A crucial finding of this study was that transcranially implanted HFMs elicited exacerbated inflammation and gliosis (as indicated by enhanced positive immunofluorescence reactivity for ED1 and GFAP). Furthermore, elevated ECM deposition and fibroblastic encapsulation were observed around the transcranially implanted HFMs. In contrast, intracranial implants (which were completely surrounded by brain tissue) elicited mitigated inflammation and gliosis. Since the transcranially implanted HFMs were in chronic contact with the meninges, the authors concluded that fibroblasts or NPCs had infiltrated into the grey matter resulting in an intense reaction.


Bridging the Divide between Neuroprosthetic Design, Tissue Engineering and Neurobiology.

Leach JB, Achyuta AK, Murthy SK - Front Neuroeng (2010)

Intensity of glial scarring in rats based on implantation procedure. (A,B) show co-expression analysis of GFAP (red) and vimentin (green) of implanted hollow fiber membranes (HFMs) in rats via two implantation schemes. Vimentin is expressed by astrocytes, microglia and fibroblasts derived from the meninges and other connective tissues. (A) Intraparenchymal implant (where the entire implant is surrounded by brain tissue) show less vimentin immunoreactivity along with GFAP reactivity. (B) Transcranial HFMs show thick layers of GFAP+/vimentin+ cells suggesting meningeal fibroblast infiltration due to skull-tethering of HFMs in such implants. The same study also showed higher ED1 reactivity in transcranial implants compared to intraparenchymal implants highlighting the exacerbated gliosis in the former implantation scheme. Scale = 100 μm. Reprinted from Kim et al. (2004). Copyright 2003, with permission from Elsevier.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2821180&req=5

Figure 6: Intensity of glial scarring in rats based on implantation procedure. (A,B) show co-expression analysis of GFAP (red) and vimentin (green) of implanted hollow fiber membranes (HFMs) in rats via two implantation schemes. Vimentin is expressed by astrocytes, microglia and fibroblasts derived from the meninges and other connective tissues. (A) Intraparenchymal implant (where the entire implant is surrounded by brain tissue) show less vimentin immunoreactivity along with GFAP reactivity. (B) Transcranial HFMs show thick layers of GFAP+/vimentin+ cells suggesting meningeal fibroblast infiltration due to skull-tethering of HFMs in such implants. The same study also showed higher ED1 reactivity in transcranial implants compared to intraparenchymal implants highlighting the exacerbated gliosis in the former implantation scheme. Scale = 100 μm. Reprinted from Kim et al. (2004). Copyright 2003, with permission from Elsevier.
Mentions: The aforementioned events are restricted to the acute and chronic response of the brain tissue upon implanting a foreign object. However, other factors such as device insertion technique [manual (Stensaas and Stensaas, 1976; Liu et al., 1999) or robotic (Maynard et al., 2000; Csicsvari et al., 2003; Nicolelis et al., 2003; Szarowski et al., 2003)], speed of insertion (Edell et al., 1992; Nicolelis et al., 2003; Bjornsson et al., 2006), and most importantly, implantation approach (Biran et al., 2007) all have been reported to affect the biological response significantly. For instance, Kim et al. (2004) elegantly compared the biological response elicited by two implantation schemes in rat cortices (Figure 6). The first scheme utilized was transcranial implantation (a practical model with respect to neuroelectrodes) of hollow fiber membranes (HFMs) and the second scheme was intracranial implantation. A crucial finding of this study was that transcranially implanted HFMs elicited exacerbated inflammation and gliosis (as indicated by enhanced positive immunofluorescence reactivity for ED1 and GFAP). Furthermore, elevated ECM deposition and fibroblastic encapsulation were observed around the transcranially implanted HFMs. In contrast, intracranial implants (which were completely surrounded by brain tissue) elicited mitigated inflammation and gliosis. Since the transcranially implanted HFMs were in chronic contact with the meninges, the authors concluded that fibroblasts or NPCs had infiltrated into the grey matter resulting in an intense reaction.

Bottom Line: Neuroprosthetic devices have made a major impact in the treatment of a variety of disorders such as paralysis and stroke.Within the context of the device-nervous system interface and central nervous system implants, areas of synergistic opportunity are discussed, including platforms to present cells with multiple cues, controlled delivery of bioactive factors, three-dimensional constructs and in vitro models of gliosis and brain injury, nerve regeneration strategies, and neural stem/progenitor cell biology.Finally, recent insights gained from the fields of developmental neurobiology and cancer biology are discussed as examples of exciting new biological knowledge that may provide fresh inspiration toward novel technologies to address the complexities associated with long-term neuroprosthetic device performance.

View Article: PubMed Central - PubMed

Affiliation: Department of Chemical and Biochemical Engineering, University of Maryland Baltimore, MD, USA.

ABSTRACT
Neuroprosthetic devices have made a major impact in the treatment of a variety of disorders such as paralysis and stroke. However, a major impediment in the advancement of this technology is the challenge of maintaining device performance during chronic implantation (months to years) due to complex intrinsic host responses such as gliosis or glial scarring. The objective of this review is to bring together research communities in neurobiology, tissue engineering, and neuroprosthetics to address the major obstacles encountered in the translation of neuroprosthetics technology into long-term clinical use. This article draws connections between specific challenges faced by current neuroprosthetics technology and recent advances in the areas of nerve tissue engineering and neurobiology. Within the context of the device-nervous system interface and central nervous system implants, areas of synergistic opportunity are discussed, including platforms to present cells with multiple cues, controlled delivery of bioactive factors, three-dimensional constructs and in vitro models of gliosis and brain injury, nerve regeneration strategies, and neural stem/progenitor cell biology. Finally, recent insights gained from the fields of developmental neurobiology and cancer biology are discussed as examples of exciting new biological knowledge that may provide fresh inspiration toward novel technologies to address the complexities associated with long-term neuroprosthetic device performance.

No MeSH data available.


Related in: MedlinePlus