TY - JOUR
T1 - Neuropharmacologic Approaches to Restore the Brain’s Microenvironment
AU - Li, Weizhe
AU - Tong, Hsin I.
AU - Gorantla, Santhi
AU - Poluektova, Larisa Y.
AU - Gendelman, Howard E.
AU - Lu, Yuanan
N1 - Funding Information:
This work was supported, in part, by the University of Nebraska Foundation, which includes but is not limited to individual donations from Carol Swarts, M.D., and Frances and Louie Blumkin, and the National Institutes of Health grants P01 DA028555, R01 NS36126, P01 NS31492, 2R01 NS034239, P01 MH64570, P01 NS43985, P30 MH062261 and R01 AG043540 (HEG); R24 OD 018546-01 (LP); and R01 MH079717 (YL). We thank the UNMC - Flow Cytometry Core facility for its help in data acquisition and analysis. We appreciate the Encapsula NanoSciences for providing the mouse artwork.
Publisher Copyright:
© 2016, Springer Science+Business Media New York.
PY - 2016/9/1
Y1 - 2016/9/1
N2 - Maintaining the central nervous system microenvironment after injury, infection, inflammatory and degenerative diseases is contingent upon adequate control of glial homeostatic functions. Disease is caused by microbial, environmental and endogenous factors that compromise ongoing nervous system functions. The final result is neuronal injury, dropout and nerve connection loss, and these underlie the pathobiology of Alzheimer’s and Parkinson’s disease, amyotrophic lateral sclerosis, stroke, and bacterial, parasitic and viral infections. However, what promotes disease are homeostatic changes in the brain’s microenvironment affected by innate glial immune pro-inflammatory and adaptive immune responses. These events disturb the brain’s metabolic activities and communication abilities. How the process affects the brain’s regulatory functions that can be harnessed for therapeutic gain is the subject at hand. Specific examples are provided that serve to modulate inflammation and improve disease outcomes specifically for HIV-associated neurocognitive disorders.
AB - Maintaining the central nervous system microenvironment after injury, infection, inflammatory and degenerative diseases is contingent upon adequate control of glial homeostatic functions. Disease is caused by microbial, environmental and endogenous factors that compromise ongoing nervous system functions. The final result is neuronal injury, dropout and nerve connection loss, and these underlie the pathobiology of Alzheimer’s and Parkinson’s disease, amyotrophic lateral sclerosis, stroke, and bacterial, parasitic and viral infections. However, what promotes disease are homeostatic changes in the brain’s microenvironment affected by innate glial immune pro-inflammatory and adaptive immune responses. These events disturb the brain’s metabolic activities and communication abilities. How the process affects the brain’s regulatory functions that can be harnessed for therapeutic gain is the subject at hand. Specific examples are provided that serve to modulate inflammation and improve disease outcomes specifically for HIV-associated neurocognitive disorders.
KW - Alzheimer’s disease
KW - Astrocytes
KW - Human immunodeficiency virus-associated neurocognitive disorders
KW - Microglia
KW - Neurodegenerative disorders
KW - Neuroinflammation
KW - Parkinson’s disease
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U2 - 10.1007/s11481-016-9686-5
DO - 10.1007/s11481-016-9686-5
M3 - Review article
C2 - 27352074
AN - SCOPUS:84976340315
VL - 11
SP - 484
EP - 494
JO - Journal of NeuroImmune Pharmacology
JF - Journal of NeuroImmune Pharmacology
SN - 1557-1890
IS - 3
ER -