The 4th Annual Meeting of the American Society for Nanomedicine

Howard E. Gendelman; Lajos P. Balogh; Raj Bawa; Michelle Bradbury; Esther H. Chang; Wah Chiu; Omid Farokhzad; Marianna Foldvari; Gregory Lanza; Kuan Wang

doi:10.1007/s11481-014-9526-4

The 4th Annual Meeting of the American Society for Nanomedicine

Howard E. Gendelman, Lajos P. Balogh, Raj Bawa, Michelle Bradbury, Esther H. Chang, Wah Chiu, Omid Farokhzad, Marianna Foldvari, Gregory Lanza, Kuan Wang

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

Abstract

The 4th Conference of the American Society for Nanomedicine is being held March 28-30, 2014 at the Universities at Shady Grove, Rockville, Maryland. The meeting's theme is on defining the role of nanomedicines for nervous system diagnostics and disease but balanced by broad and timely topics for nanotechnology. Nanoneuromedicine, as defined by the development of small drug formulations for the diagnosis and treatment of degenerative, inflammatory, infectious, vascular, addictive, behavioral and metabolic disorders of the nervous system, will provide a focus for each of the scientific sessions. This research is interdisciplinary and it's in its infancy. The hurdles that preclude translation from bench to bedside would include its delivery across the blood brain barrier, limiting nervous system toxicities, and improving drug targeting to diseased brain subregions. These all pose challenges. Multidisciplinary works in neuroscience (neurobiology, neurochemistry, neurophysiology, and neuroinflammation), bioimaging, and polymer chemistry to facilitate outcomes for formulation manufacture will be vigorously discussed. How drugs reach sites of action need include neural cell specific subcellular compartments. The ASNM meeting will showcase nanoneuromedicine research from leading investigators of divergent scientific backgrounds who define this new field. It will also serve as an incubator for developing investigators and broad new field discoveries. Welcome to the conference and enjoy!

Original language	English
Pages (from-to)	S1-S38
Journal	Journal of Neuroimmune Pharmacology
Volume	9
Issue number	SUPPL. 1
DOIs	https://doi.org/10.1007/s11481-014-9526-4
State	Published - Mar 2014

Keywords

Blood Brain Barrier; Product translation
Diagnostics
Drug targeting
Nanomedicine
Nanotoxicity
Neuroimaging
Neurotherapeutics

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10.1007/s11481-014-9526-4

Cite this

@article{24535b4071bf432588aac780804515f2,

title = "The 4th Annual Meeting of the American Society for Nanomedicine",

abstract = "The 4th Conference of the American Society for Nanomedicine is being held March 28-30, 2014 at the Universities at Shady Grove, Rockville, Maryland. The meeting's theme is on defining the role of nanomedicines for nervous system diagnostics and disease but balanced by broad and timely topics for nanotechnology. Nanoneuromedicine, as defined by the development of small drug formulations for the diagnosis and treatment of degenerative, inflammatory, infectious, vascular, addictive, behavioral and metabolic disorders of the nervous system, will provide a focus for each of the scientific sessions. This research is interdisciplinary and it's in its infancy. The hurdles that preclude translation from bench to bedside would include its delivery across the blood brain barrier, limiting nervous system toxicities, and improving drug targeting to diseased brain subregions. These all pose challenges. Multidisciplinary works in neuroscience (neurobiology, neurochemistry, neurophysiology, and neuroinflammation), bioimaging, and polymer chemistry to facilitate outcomes for formulation manufacture will be vigorously discussed. How drugs reach sites of action need include neural cell specific subcellular compartments. The ASNM meeting will showcase nanoneuromedicine research from leading investigators of divergent scientific backgrounds who define this new field. It will also serve as an incubator for developing investigators and broad new field discoveries. Welcome to the conference and enjoy!",

keywords = "Blood Brain Barrier; Product translation, Diagnostics, Drug targeting, Nanomedicine, Nanotoxicity, Neuroimaging, Neurotherapeutics",

author = "Gendelman, {Howard E.} and Balogh, {Lajos P.} and Raj Bawa and Michelle Bradbury and Chang, {Esther H.} and Wah Chiu and Omid Farokhzad and Marianna Foldvari and Gregory Lanza and Kuan Wang",

note = "Funding Information: The conference was supported by the National Institutes of Health, National Institute of Neurological Disorders and Stroke R13 Scientific Conference grant 1R13NS083315-01; Seton Hall University; UNMC; Carol Swarts, MD, Emerging Neuroscience Research Laboratory, UNMC; ViiV Healthcare Company; Springer publisher, Journal of Neuroimmune Pharmacology. Funding Information: based strategies can significantly impact peripheral nerve regeneration as well. Schwann cells, in conjunction with micropatterned substrates, have been shown to secrete nerve growth factor and facilitate peripheral nerve regeneration. In order to facilitate peripheral nerve regeneration, polymeric conduits with micro/nanopatterns were fabricated and the transdifferentiation of mesenchymal stem cells to Schwann-cell like phenotypes was investigated. This talk will therefore highlight the importance of nanomedicine in both peripheral and central nervous system regeneration. Supported by: US Army Grant No. W81XWH-10-1-0806 Funding Information: Traumatic brain injury (TBI) affects neural cells and cerebral vasculature integrity leading to progressive neurodegenera-tion. The innate and adaptive immune systems respond to such injury leading to facilitated damage and repair. The balance between T effector (Teff) and regulatory T cell (Treg) functions can regulate neuroinflammatory responses at sites of tissue damage. Here, Teff accelerate while Treg restrict continued tissue damage. These actions suggest that Tregs may be harnessed to positively affect disease outcomes and for targeted drug delivery. To facilitate a Treg protective immune response, we subjected C57BL/6 mice to a controlled cortical impact. The mice were randomized to receive either granulocyte macrophage colony stimulating factor (GM-CSF; 50 μg/kg), a hematopoietic stem cell factor and known Treg inducer, or an equal volume of saline 6 h after injury then continued daily until sacrifice (7 or 14 days). GM-CSF modestly increased splenic Treg populations. Sparing of cortical tissue was seen after GM-CSF administration with untreated animals having lesions ~10–15 % larger than treated animals. Staining for ionized calcium binding adaptor molecule 1, a microglia marker, was seen at the lesion site as well as the surrounding regions on days 7 and 14. GM-CSF significantly decreased staining and appeared to alter microglia morphology. Immunoreactivity for glial fibrillary acidic protein, an astrocyte marker, did not differ amongst treatment groups. As GM-CSF administration can elicit neuroprotection, we theorized the Treg could be used as a drug carrier and notably for vascular endothelial growth factor (VEGF) which shows angiogenic and neuroprotective properties following TBI. Therefore, we hypothesized that T cell targeted delivery of a VEGF complex prepared using anionic block copolymers of poly(ethylene oxide)-block-poly(L-glutamic acid) could provide synergistic protection to an injured vasculature and parenchyma. Supported by: Carol Swarts Neuroscience Research Laboratory, the Frances and Louie Blumkin Foundation, Department of Defense Grant W81XWH11-1-0700, and National Institutes of Health grants P20 GM103480, P01 DA028555, R01 NS36126, P01 NS31492, 2R01 NS034239, P01 MH64570 and P01 NS43985. Funding Information: Drug toxicities, patient compliance and limited penetrance into viral reservoirs have diminished long-term antiretroviral therapy (ART) efficacy. Novel strategies serve to improve ART delivery to mononuclear phagocytes (MP: monocytes and tissue macrophages) and CD4+ T lymphocytes to bring drugs to viral reservoirs. Over the past decade we pioneered the development of long-acting injectable nanoformulated ART (nanoART) with superior pharmacokinetics. A “Trojan Horse” MP carriage of the drug formulations facilitated the development of long-lived storage depots, in liver and spleen. Our drug formulations enable drug transfer to an infected CNS. We are currently improving nanoART technology to move it to human use. We maximized viral clearance by developing a range of antiretroviral nanoformulated drugs. Synthesis of polymer drugs with attachments of specific ligand coating directed drugs to specific virus{\textquoteright} target cells and subcellular regions to optimize antiretroviral activities. We probed directed formulations in rodents using a newly discovered small magnetite ART (SMART) platform. SMART formulations were synthesized by crystalline particles and evaluated for drug pharmacokinetics. Histologic and imaging assays evaluated drug toxicities. Drug polymer formulations were tested for antiretroviral efficacy, immune and neuroprotection in a humanized mouse model of HIV infection. The work improves nanoART towards the goal of viral eradication. Supported by: NIH R01 AG043540-01A1, P01 DA028555-04, R01 NS3439-19 (HEG). Funding Information: Supported by: NIH P01DA028555, R01NS036126, R01NS34239 (HEG) Funding Information: Macrophages play an important role in atherosclerotic lesion progression by facilitating cholesterol accumulation and increasing inflammatory responses in aortic walls. After accumulating cholesterol, macrophages can be transformed into foam cells, which characterize the atherosclerotic lesion. (-)-Epigallocatechin gallate (EGCG), a natural compound found in green tea, has a potential to inhibit foam cells formation through decreasing macrophages cholesterol accumulation and inflammatory response. We have successfully synthesized targeted EGCG loaded lipid nanoparticles (T-nanoE). The EGCG stability was significantly increased by the nanoparticles. T-nanoE had higher binding affinity to macrophages than non-targeted EGCG loaded lipid nanoparticles (nanoE). After knocking down a scavenger receptor, T-nanoE had a low binding affinity to macrophages. As compared to native EGCG, EGCG nanoparticles significantly decreased macrophage cholesteryl ester content measured using a high perfor- mance liquid chromatography (HPLC) system. EGCG nanoparticles also decreased the expression of monocyte chemoattractant protein 1 (MCP-1) in macrophages. In conclusion, lipid nanoparticles increase EGCG stability. T-nanoE can target to macrophages. Both T-nanoE and nanoE inhibit foam cell formation. T-nanoE might be better than nanoE. Supported by: NIH NCCAM Grant Number R15AT007013 Funding Information: Progressive HIV infection commonly leads to cognitive impairments for HIV associated neurocognitive disorders. Our labs have successfully reproduced the biology, immunology and virology of HAND in mice. This is timely as, no reliable diagnostic test for human disease is available and disease tracking and therapeutic monitoring are not available in animal models. We believe we have found an answer to this bottleneck. To this end, we recently developed a manganese enhanced MRI (MEMRI) method to reflect central nervous system damage following HIV infection. This is based on the abilities of Mn2+ acting as a calcium analog where it enters into neurons through calcium channels. Thus, the T1 relaxivity changes, and hence T1 weighted signal intensity, are quantitatively proportional to calcium channel Mn2+ activities. MEMRI was used to examine brains of humanized mice infected by HIV-1. Changes in MEMRI signal enhancements during HIV-1 infection showed profound changes in Mn2+ accumulation suggesting associated neural pathology. This was observed in disease affected brain regions. Multiple linear regression analysis showed changed MEMRI signal enhancements positively correlated with high viral loads at study end (r=0.78 p<0.05) and negatively with peripheral CD4+ T cells (r=-0.437 p<0.05). Quantitative immunohistological results showed that GFAP reactions correlated positively with signal enhancements in CA1 (r=0.96, p<0.05), CA3 (r=0.89, p<0.5) and the dentate gyrus (r= 0.95, p<0.05). This was negatively correlated with synaptophysin in the CA3 (r=-0.98 p=<0.05) and the sensory regions of cortex (r=-0.87, p=0.05). The abnormal signal intensity correlated with viral pathology in infected mice supporting the emergence of behavioral deficits in infected animals. We conclude MEMRI could be used to investigate specific neuropathologic aberrations associated with advanced viral infection and can be used to monitor therapeutic efficacy to combat neuronal damage in HAND. Supported by: NIH P01DA028555, R01NS036126, R01NS34239 (HEG) Funding Information: Mycobacterium tuberculosis (MTB) is the cause of wide-spread pulmonary, bone, nervous system, skin, eye and other systemic morbidities. Complex drug regimens underlie an alarming worldwide increase in infection rates. The needs for new treatment regimens to improve patient compliance and speed microbial eradication are surely needed. We posit that this may be achieved through long-acting, cell and tissue targeted, nanoformulated MTB medicines. To this end, we developed a derivatized hydrophobic isoniazid now called INHP. INHP and rifampin (RIF) were loaded into poly-lactide-coglycolic acid (PLGA) nanoparticles. Physical and chemical properties of the drug formulations as well as the resultant particle cell uptake, retention, viability and antimicrobial efficacy were determined in relationship to native drugs. These nanoformulations displayed enhanced uptake of 6 and 4 μg of drug/106 cells when compared to 0.1 μg/ 106 cells for native drugs. Sustained release of encapsulated INHP and RIF were detectable in monocyte-derived macrophages (MDM) over 15 days whereas native drug was released within 24 h. Antimicrobial activities as determined in dose response tests against Mycobacterium smegmatis showed ~6-fold increases over equivalent concentration of native drug when both INHP and RIF nanoformulations were administered together. Endocytic trafficking of the antimycobacterium nanoparticles and M. smegmatis showed identical subcellular compartment localization in recycling and late endosomes. In conclusion, PLGA nanoparticles encapsulating RIF and INHP significantly improves drug uptake and retention and antimicrobial activities from native drugs. Subcellular distribution study of M. smegmatis and the PLGA nanoformulations show that the drugs and the mycobacterium are trafficked into equivalent endocytic compartments. These results highlight new opportunities for antimicrobial nanomedicines to simplify and improve the means to affect MTB eradication. Supported by: NIH P01DA028555 and R01 A1097550 (HEG) Funding Information: Supported by: This project is part of the joint venture supported by Intramural to India (I-to-I) funding for treatment and prevention of sexually transmitted diseases awarded to Dr. Anu Puri (NCI) and Dr. K.P. Singh (Pantnagar University).",

year = "2014",

month = mar,

doi = "10.1007/s11481-014-9526-4",

language = "English",

volume = "9",

pages = "S1--S38",

journal = "Journal of Neuroimmune Pharmacology",

issn = "1557-1890",

number = "SUPPL. 1",

}

TY - JOUR

T1 - The 4th Annual Meeting of the American Society for Nanomedicine

AU - Gendelman, Howard E.

AU - Balogh, Lajos P.

AU - Bawa, Raj

AU - Bradbury, Michelle

AU - Chang, Esther H.

AU - Chiu, Wah

AU - Farokhzad, Omid

AU - Foldvari, Marianna

AU - Lanza, Gregory

AU - Wang, Kuan

N1 - Funding Information: The conference was supported by the National Institutes of Health, National Institute of Neurological Disorders and Stroke R13 Scientific Conference grant 1R13NS083315-01; Seton Hall University; UNMC; Carol Swarts, MD, Emerging Neuroscience Research Laboratory, UNMC; ViiV Healthcare Company; Springer publisher, Journal of Neuroimmune Pharmacology. Funding Information: based strategies can significantly impact peripheral nerve regeneration as well. Schwann cells, in conjunction with micropatterned substrates, have been shown to secrete nerve growth factor and facilitate peripheral nerve regeneration. In order to facilitate peripheral nerve regeneration, polymeric conduits with micro/nanopatterns were fabricated and the transdifferentiation of mesenchymal stem cells to Schwann-cell like phenotypes was investigated. This talk will therefore highlight the importance of nanomedicine in both peripheral and central nervous system regeneration. Supported by: US Army Grant No. W81XWH-10-1-0806 Funding Information: Traumatic brain injury (TBI) affects neural cells and cerebral vasculature integrity leading to progressive neurodegenera-tion. The innate and adaptive immune systems respond to such injury leading to facilitated damage and repair. The balance between T effector (Teff) and regulatory T cell (Treg) functions can regulate neuroinflammatory responses at sites of tissue damage. Here, Teff accelerate while Treg restrict continued tissue damage. These actions suggest that Tregs may be harnessed to positively affect disease outcomes and for targeted drug delivery. To facilitate a Treg protective immune response, we subjected C57BL/6 mice to a controlled cortical impact. The mice were randomized to receive either granulocyte macrophage colony stimulating factor (GM-CSF; 50 μg/kg), a hematopoietic stem cell factor and known Treg inducer, or an equal volume of saline 6 h after injury then continued daily until sacrifice (7 or 14 days). GM-CSF modestly increased splenic Treg populations. Sparing of cortical tissue was seen after GM-CSF administration with untreated animals having lesions ~10–15 % larger than treated animals. Staining for ionized calcium binding adaptor molecule 1, a microglia marker, was seen at the lesion site as well as the surrounding regions on days 7 and 14. GM-CSF significantly decreased staining and appeared to alter microglia morphology. Immunoreactivity for glial fibrillary acidic protein, an astrocyte marker, did not differ amongst treatment groups. As GM-CSF administration can elicit neuroprotection, we theorized the Treg could be used as a drug carrier and notably for vascular endothelial growth factor (VEGF) which shows angiogenic and neuroprotective properties following TBI. Therefore, we hypothesized that T cell targeted delivery of a VEGF complex prepared using anionic block copolymers of poly(ethylene oxide)-block-poly(L-glutamic acid) could provide synergistic protection to an injured vasculature and parenchyma. Supported by: Carol Swarts Neuroscience Research Laboratory, the Frances and Louie Blumkin Foundation, Department of Defense Grant W81XWH11-1-0700, and National Institutes of Health grants P20 GM103480, P01 DA028555, R01 NS36126, P01 NS31492, 2R01 NS034239, P01 MH64570 and P01 NS43985. Funding Information: Drug toxicities, patient compliance and limited penetrance into viral reservoirs have diminished long-term antiretroviral therapy (ART) efficacy. Novel strategies serve to improve ART delivery to mononuclear phagocytes (MP: monocytes and tissue macrophages) and CD4+ T lymphocytes to bring drugs to viral reservoirs. Over the past decade we pioneered the development of long-acting injectable nanoformulated ART (nanoART) with superior pharmacokinetics. A “Trojan Horse” MP carriage of the drug formulations facilitated the development of long-lived storage depots, in liver and spleen. Our drug formulations enable drug transfer to an infected CNS. We are currently improving nanoART technology to move it to human use. We maximized viral clearance by developing a range of antiretroviral nanoformulated drugs. Synthesis of polymer drugs with attachments of specific ligand coating directed drugs to specific virus’ target cells and subcellular regions to optimize antiretroviral activities. We probed directed formulations in rodents using a newly discovered small magnetite ART (SMART) platform. SMART formulations were synthesized by crystalline particles and evaluated for drug pharmacokinetics. Histologic and imaging assays evaluated drug toxicities. Drug polymer formulations were tested for antiretroviral efficacy, immune and neuroprotection in a humanized mouse model of HIV infection. The work improves nanoART towards the goal of viral eradication. Supported by: NIH R01 AG043540-01A1, P01 DA028555-04, R01 NS3439-19 (HEG). Funding Information: Supported by: NIH P01DA028555, R01NS036126, R01NS34239 (HEG) Funding Information: Macrophages play an important role in atherosclerotic lesion progression by facilitating cholesterol accumulation and increasing inflammatory responses in aortic walls. After accumulating cholesterol, macrophages can be transformed into foam cells, which characterize the atherosclerotic lesion. (-)-Epigallocatechin gallate (EGCG), a natural compound found in green tea, has a potential to inhibit foam cells formation through decreasing macrophages cholesterol accumulation and inflammatory response. We have successfully synthesized targeted EGCG loaded lipid nanoparticles (T-nanoE). The EGCG stability was significantly increased by the nanoparticles. T-nanoE had higher binding affinity to macrophages than non-targeted EGCG loaded lipid nanoparticles (nanoE). After knocking down a scavenger receptor, T-nanoE had a low binding affinity to macrophages. As compared to native EGCG, EGCG nanoparticles significantly decreased macrophage cholesteryl ester content measured using a high perfor- mance liquid chromatography (HPLC) system. EGCG nanoparticles also decreased the expression of monocyte chemoattractant protein 1 (MCP-1) in macrophages. In conclusion, lipid nanoparticles increase EGCG stability. T-nanoE can target to macrophages. Both T-nanoE and nanoE inhibit foam cell formation. T-nanoE might be better than nanoE. Supported by: NIH NCCAM Grant Number R15AT007013 Funding Information: Progressive HIV infection commonly leads to cognitive impairments for HIV associated neurocognitive disorders. Our labs have successfully reproduced the biology, immunology and virology of HAND in mice. This is timely as, no reliable diagnostic test for human disease is available and disease tracking and therapeutic monitoring are not available in animal models. We believe we have found an answer to this bottleneck. To this end, we recently developed a manganese enhanced MRI (MEMRI) method to reflect central nervous system damage following HIV infection. This is based on the abilities of Mn2+ acting as a calcium analog where it enters into neurons through calcium channels. Thus, the T1 relaxivity changes, and hence T1 weighted signal intensity, are quantitatively proportional to calcium channel Mn2+ activities. MEMRI was used to examine brains of humanized mice infected by HIV-1. Changes in MEMRI signal enhancements during HIV-1 infection showed profound changes in Mn2+ accumulation suggesting associated neural pathology. This was observed in disease affected brain regions. Multiple linear regression analysis showed changed MEMRI signal enhancements positively correlated with high viral loads at study end (r=0.78 p<0.05) and negatively with peripheral CD4+ T cells (r=-0.437 p<0.05). Quantitative immunohistological results showed that GFAP reactions correlated positively with signal enhancements in CA1 (r=0.96, p<0.05), CA3 (r=0.89, p<0.5) and the dentate gyrus (r= 0.95, p<0.05). This was negatively correlated with synaptophysin in the CA3 (r=-0.98 p=<0.05) and the sensory regions of cortex (r=-0.87, p=0.05). The abnormal signal intensity correlated with viral pathology in infected mice supporting the emergence of behavioral deficits in infected animals. We conclude MEMRI could be used to investigate specific neuropathologic aberrations associated with advanced viral infection and can be used to monitor therapeutic efficacy to combat neuronal damage in HAND. Supported by: NIH P01DA028555, R01NS036126, R01NS34239 (HEG) Funding Information: Mycobacterium tuberculosis (MTB) is the cause of wide-spread pulmonary, bone, nervous system, skin, eye and other systemic morbidities. Complex drug regimens underlie an alarming worldwide increase in infection rates. The needs for new treatment regimens to improve patient compliance and speed microbial eradication are surely needed. We posit that this may be achieved through long-acting, cell and tissue targeted, nanoformulated MTB medicines. To this end, we developed a derivatized hydrophobic isoniazid now called INHP. INHP and rifampin (RIF) were loaded into poly-lactide-coglycolic acid (PLGA) nanoparticles. Physical and chemical properties of the drug formulations as well as the resultant particle cell uptake, retention, viability and antimicrobial efficacy were determined in relationship to native drugs. These nanoformulations displayed enhanced uptake of 6 and 4 μg of drug/106 cells when compared to 0.1 μg/ 106 cells for native drugs. Sustained release of encapsulated INHP and RIF were detectable in monocyte-derived macrophages (MDM) over 15 days whereas native drug was released within 24 h. Antimicrobial activities as determined in dose response tests against Mycobacterium smegmatis showed ~6-fold increases over equivalent concentration of native drug when both INHP and RIF nanoformulations were administered together. Endocytic trafficking of the antimycobacterium nanoparticles and M. smegmatis showed identical subcellular compartment localization in recycling and late endosomes. In conclusion, PLGA nanoparticles encapsulating RIF and INHP significantly improves drug uptake and retention and antimicrobial activities from native drugs. Subcellular distribution study of M. smegmatis and the PLGA nanoformulations show that the drugs and the mycobacterium are trafficked into equivalent endocytic compartments. These results highlight new opportunities for antimicrobial nanomedicines to simplify and improve the means to affect MTB eradication. Supported by: NIH P01DA028555 and R01 A1097550 (HEG) Funding Information: Supported by: This project is part of the joint venture supported by Intramural to India (I-to-I) funding for treatment and prevention of sexually transmitted diseases awarded to Dr. Anu Puri (NCI) and Dr. K.P. Singh (Pantnagar University).

PY - 2014/3

Y1 - 2014/3

N2 - The 4th Conference of the American Society for Nanomedicine is being held March 28-30, 2014 at the Universities at Shady Grove, Rockville, Maryland. The meeting's theme is on defining the role of nanomedicines for nervous system diagnostics and disease but balanced by broad and timely topics for nanotechnology. Nanoneuromedicine, as defined by the development of small drug formulations for the diagnosis and treatment of degenerative, inflammatory, infectious, vascular, addictive, behavioral and metabolic disorders of the nervous system, will provide a focus for each of the scientific sessions. This research is interdisciplinary and it's in its infancy. The hurdles that preclude translation from bench to bedside would include its delivery across the blood brain barrier, limiting nervous system toxicities, and improving drug targeting to diseased brain subregions. These all pose challenges. Multidisciplinary works in neuroscience (neurobiology, neurochemistry, neurophysiology, and neuroinflammation), bioimaging, and polymer chemistry to facilitate outcomes for formulation manufacture will be vigorously discussed. How drugs reach sites of action need include neural cell specific subcellular compartments. The ASNM meeting will showcase nanoneuromedicine research from leading investigators of divergent scientific backgrounds who define this new field. It will also serve as an incubator for developing investigators and broad new field discoveries. Welcome to the conference and enjoy!

AB - The 4th Conference of the American Society for Nanomedicine is being held March 28-30, 2014 at the Universities at Shady Grove, Rockville, Maryland. The meeting's theme is on defining the role of nanomedicines for nervous system diagnostics and disease but balanced by broad and timely topics for nanotechnology. Nanoneuromedicine, as defined by the development of small drug formulations for the diagnosis and treatment of degenerative, inflammatory, infectious, vascular, addictive, behavioral and metabolic disorders of the nervous system, will provide a focus for each of the scientific sessions. This research is interdisciplinary and it's in its infancy. The hurdles that preclude translation from bench to bedside would include its delivery across the blood brain barrier, limiting nervous system toxicities, and improving drug targeting to diseased brain subregions. These all pose challenges. Multidisciplinary works in neuroscience (neurobiology, neurochemistry, neurophysiology, and neuroinflammation), bioimaging, and polymer chemistry to facilitate outcomes for formulation manufacture will be vigorously discussed. How drugs reach sites of action need include neural cell specific subcellular compartments. The ASNM meeting will showcase nanoneuromedicine research from leading investigators of divergent scientific backgrounds who define this new field. It will also serve as an incubator for developing investigators and broad new field discoveries. Welcome to the conference and enjoy!

KW - Blood Brain Barrier; Product translation

KW - Diagnostics

KW - Drug targeting

KW - Nanomedicine

KW - Nanotoxicity

KW - Neuroimaging

KW - Neurotherapeutics

UR - http://www.scopus.com/inward/record.url?scp=84899414260&partnerID=8YFLogxK

U2 - 10.1007/s11481-014-9526-4

DO - 10.1007/s11481-014-9526-4

M3 - Article

C2 - 24550132

AN - SCOPUS:84899414260

SN - 1557-1890

VL - 9

SP - S1-S38

JO - Journal of Neuroimmune Pharmacology

JF - Journal of Neuroimmune Pharmacology

IS - SUPPL. 1

ER -

The 4th Annual Meeting of the American Society for Nanomedicine

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Keywords

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