By Olimpia Meucci (auth.), Olimpia Meucci (eds.)
Chemokines and their receptors are being well-known as an critical component to the frightened process implicated in primary elements of improvement and homeostasis, similar to neurotransmission, proliferation, differentiation, and neuronal-glial communique. therefore, their involvement in HIV neuropathology is going a long way past the co-receptors function and involves complicated interactions of the chemokine approach with diversified mobilephone forms and different regulators of neuronal functionality. the main target of this quantity is to study those issues which will spotlight changes of chemokine body structure which could give a contribution to neuroAIDS and different neuropathologies.
This e-book could be of curiosity to neuroscientists, neurologists, virologists, pharmacologists, and scholars in those fields.
About the Editor:
Olimpia Meucci, MD, PhD is a Professor of Pharmacology and body structure & Microbiology and Immunology at Drexel college collage of medication in Philadelphia, PA. given that her seminal discovery in regards to the rules of neuronal signaling by way of chemokines, her learn has essentially all for the physio-pathological roles of this crucial category of neuroimmune modulators within the critical anxious procedure and their involvement in neuroAIDS. those stories have considerably contributed to present realizing of the mobile and molecular mechanisms of HIV-related neuropathology together with the interplay of the chemokine approach with drug of abuse, specifically opiates, which remains to be an enormous sector of research within the Meucci lab.
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Extra info for Chemokine Receptors and NeuroAIDS: Beyond Co-Receptor Function and Links to Other Neuropathologies
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Like glutamate, QUIN levels are shown to be elevated in CSF and brain parenchyma of HIV-infected patients and those with other CNS infections (Heyes et al. 1991; Heyes et al. 2001) (Achim et al. 1993). The accumulation of these excitatory amines points to malfunctioning glia cells since microglia are predominate producers of QUIN while both microglia and astrocytes regulate extracellular glutamate levels. QUIN and glutamate are metabolically processed by microglia and astrocytes and inflammatory mediators can alter the normal processing of these amines resulting in their accumulation in the extracellular space.
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