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

Immunoreactive cellular stratification at the brain-neuroelectrode interface examined using cell-specific markers in a histological section of a rodent brain following a 4-week microlectrode implantation. Microglial (ED1+; red) proximity to the immediate vicinity of the probe indicates inflammation. Scar-like astrocytes (GFAP+; green) with interwoven processes indicate anisomorphic gliosis. The area of inflammation and intense astrocytic reactivity has a reduced number of neurons, indicated by NeuN+ (blue) and neurofilament+ (purple) cells indicating loss of connectivity between the probe and the neurons following 4 weeks of implantation. The neuroelectrode position is illustrated by an orange patch on the left side of the image. Reprinted from Biran et al. (2005). Copyright 2005, with permission from Elsevier.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Immunoreactive cellular stratification at the brain-neuroelectrode interface examined using cell-specific markers in a histological section of a rodent brain following a 4-week microlectrode implantation. Microglial (ED1+; red) proximity to the immediate vicinity of the probe indicates inflammation. Scar-like astrocytes (GFAP+; green) with interwoven processes indicate anisomorphic gliosis. The area of inflammation and intense astrocytic reactivity has a reduced number of neurons, indicated by NeuN+ (blue) and neurofilament+ (purple) cells indicating loss of connectivity between the probe and the neurons following 4 weeks of implantation. The neuroelectrode position is illustrated by an orange patch on the left side of the image. Reprinted from Biran et al. (2005). Copyright 2005, with permission from Elsevier.

Mentions: The first event that occurs in the chronic reaction, and one that probably persists throughout the duration of the presence of implant, is the attachment and clustering of microglia on the implant surface (Stensaas and Stensaas, 1976; Winn et al., 1989; Mofid et al., 1997; Kao et al., 1999), as shown in Figure 5. This attachment is thought to be mediated by the adsorption of serum on the implant surface or due to the release of chemo-attractants by serum factors such as monocytes chemotactic protein-1 (MCP 1) and macrophage inflammatory protein (MIP-1) at injury sites (Saadoun et al., 2005). Following colonization, these cells try to degrade and remove the implant by secreting lytic enzymes and reactive oxygen species (Kyrkanides et al., 2001; Takeuchi et al., 2001). The action of these cells is analogous to that of peripherally derived macrophages that fuse into giant multi-nucleated cells to degrade foreign objects (Stensaas and Stensaas, 1976). In addition, microglia are also known to produce cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) that may result in astrocyte activation (Merrill and Benveniste, 1996; John et al., 2005). Furthermore, microglia have been postulated to regulate the production of the basal lamina, a thin sheet comprising extracellular matrix (ECM) proteins, that aids in organizing the glial scar (Polikov, 2009). The proteins in this basal lamina can act synergistically to present a substrate for cellular attachment via laminin and collagen (Alberts et al., 2001).


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

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

Immunoreactive cellular stratification at the brain-neuroelectrode interface examined using cell-specific markers in a histological section of a rodent brain following a 4-week microlectrode implantation. Microglial (ED1+; red) proximity to the immediate vicinity of the probe indicates inflammation. Scar-like astrocytes (GFAP+; green) with interwoven processes indicate anisomorphic gliosis. The area of inflammation and intense astrocytic reactivity has a reduced number of neurons, indicated by NeuN+ (blue) and neurofilament+ (purple) cells indicating loss of connectivity between the probe and the neurons following 4 weeks of implantation. The neuroelectrode position is illustrated by an orange patch on the left side of the image. Reprinted from Biran et al. (2005). Copyright 2005, with permission from Elsevier.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Immunoreactive cellular stratification at the brain-neuroelectrode interface examined using cell-specific markers in a histological section of a rodent brain following a 4-week microlectrode implantation. Microglial (ED1+; red) proximity to the immediate vicinity of the probe indicates inflammation. Scar-like astrocytes (GFAP+; green) with interwoven processes indicate anisomorphic gliosis. The area of inflammation and intense astrocytic reactivity has a reduced number of neurons, indicated by NeuN+ (blue) and neurofilament+ (purple) cells indicating loss of connectivity between the probe and the neurons following 4 weeks of implantation. The neuroelectrode position is illustrated by an orange patch on the left side of the image. Reprinted from Biran et al. (2005). Copyright 2005, with permission from Elsevier.
Mentions: The first event that occurs in the chronic reaction, and one that probably persists throughout the duration of the presence of implant, is the attachment and clustering of microglia on the implant surface (Stensaas and Stensaas, 1976; Winn et al., 1989; Mofid et al., 1997; Kao et al., 1999), as shown in Figure 5. This attachment is thought to be mediated by the adsorption of serum on the implant surface or due to the release of chemo-attractants by serum factors such as monocytes chemotactic protein-1 (MCP 1) and macrophage inflammatory protein (MIP-1) at injury sites (Saadoun et al., 2005). Following colonization, these cells try to degrade and remove the implant by secreting lytic enzymes and reactive oxygen species (Kyrkanides et al., 2001; Takeuchi et al., 2001). The action of these cells is analogous to that of peripherally derived macrophages that fuse into giant multi-nucleated cells to degrade foreign objects (Stensaas and Stensaas, 1976). In addition, microglia are also known to produce cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) that may result in astrocyte activation (Merrill and Benveniste, 1996; John et al., 2005). Furthermore, microglia have been postulated to regulate the production of the basal lamina, a thin sheet comprising extracellular matrix (ECM) proteins, that aids in organizing the glial scar (Polikov, 2009). The proteins in this basal lamina can act synergistically to present a substrate for cellular attachment via laminin and collagen (Alberts et al., 2001).

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