Limits...
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

Glial scar ultrastructure within adult rat spinal cord as revealed by GFAP staining. (A) Astrocytes in normal uninjured thoracic spinal cord. (B) Isomorphic gliosis showing tissue surrounding GFAP positive astrocytes (arrows) is much less disturbed following a lacerating injury (out of frame). (C) Anisomorphic gliosis showing a dense scar tissue composed of activated astrocytes with interlocking processes encapsulating the damaged region of CNS (to the left of the frame is a spinal lesion). Scale = 20 μm. Figure adapted from McGraw et al. (2001). Copyright 2001 Wiley & Co. Reproduced with permission.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC2821180&req=5

Figure 4: Glial scar ultrastructure within adult rat spinal cord as revealed by GFAP staining. (A) Astrocytes in normal uninjured thoracic spinal cord. (B) Isomorphic gliosis showing tissue surrounding GFAP positive astrocytes (arrows) is much less disturbed following a lacerating injury (out of frame). (C) Anisomorphic gliosis showing a dense scar tissue composed of activated astrocytes with interlocking processes encapsulating the damaged region of CNS (to the left of the frame is a spinal lesion). Scale = 20 μm. Figure adapted from McGraw et al. (2001). Copyright 2001 Wiley & Co. Reproduced with permission.

Mentions: Once the acute reaction subsides, the chronic reaction is initiated due to the persistent presence of an insoluble foreign material (Landis, 1994; Fawcett and Asher, 1999; Turner et al., 1999; Szarowski et al., 2003; Biran et al., 2005; Polikov et al., 2005; Polikov, 2009). This reaction is a complex cascade of events characterized by continued inflammation, adhesion of activated microglia on the probe surface, astrocyte activation, and the formation of glial/fibrotic scar tissue that surrounds and insulates the probe (Turner et al., 1999; Szarowski et al., 2003; Polikov et al., 2005; Brazda and Muller, 2009). Figure 4 shows the characteristic glial scarring response that follows after spinal cord injury in a rat.


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

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

Glial scar ultrastructure within adult rat spinal cord as revealed by GFAP staining. (A) Astrocytes in normal uninjured thoracic spinal cord. (B) Isomorphic gliosis showing tissue surrounding GFAP positive astrocytes (arrows) is much less disturbed following a lacerating injury (out of frame). (C) Anisomorphic gliosis showing a dense scar tissue composed of activated astrocytes with interlocking processes encapsulating the damaged region of CNS (to the left of the frame is a spinal lesion). Scale = 20 μm. Figure adapted from McGraw et al. (2001). Copyright 2001 Wiley & Co. Reproduced with permission.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: Glial scar ultrastructure within adult rat spinal cord as revealed by GFAP staining. (A) Astrocytes in normal uninjured thoracic spinal cord. (B) Isomorphic gliosis showing tissue surrounding GFAP positive astrocytes (arrows) is much less disturbed following a lacerating injury (out of frame). (C) Anisomorphic gliosis showing a dense scar tissue composed of activated astrocytes with interlocking processes encapsulating the damaged region of CNS (to the left of the frame is a spinal lesion). Scale = 20 μm. Figure adapted from McGraw et al. (2001). Copyright 2001 Wiley & Co. Reproduced with permission.
Mentions: Once the acute reaction subsides, the chronic reaction is initiated due to the persistent presence of an insoluble foreign material (Landis, 1994; Fawcett and Asher, 1999; Turner et al., 1999; Szarowski et al., 2003; Biran et al., 2005; Polikov et al., 2005; Polikov, 2009). This reaction is a complex cascade of events characterized by continued inflammation, adhesion of activated microglia on the probe surface, astrocyte activation, and the formation of glial/fibrotic scar tissue that surrounds and insulates the probe (Turner et al., 1999; Szarowski et al., 2003; Polikov et al., 2005; Brazda and Muller, 2009). Figure 4 shows the characteristic glial scarring response that follows after spinal cord injury in a rat.

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