Abstract
The use of methamphetamine is steadily increasing worldwide. Its use is associated with high-risk sexual behavior and subsequent infection with HIV. Methamphetamine has profound effects on the brain both as an acute intoxicant and following chronic exposure. The combined effects of HIV and methamphetamine appear to result in widespread neuronal and white matter injury. These changes are most prominent in the basal ganglia and frontal lobe, and are not restricted to dopaminergic neurons. Additionally, methamphetamine and HIV proteins disrupt the blood brain barrier, cause glial cell activation and impair the function of neural progenitor cells. Methamphetamine also results in increased HIV replication via activation of chemokine receptors involved in HIV entry. Common pathways in several of these effects seem to involve induction of oxidative stress. Characterization of these subcellular pathways and identification of common targets is essential for development of therapeutic strategies for HIV-infected methamphetamine abusers.
Keywords: HIV, AIDS, methamphetamine, brain, neuron, dopamine, Tat, gp120
Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry
Title: Methamphetamine and HIV Infection, Role in Neurocognitive Dysfunction
Volume: 8 Issue: 2
Author(s): Katherine Conant, Arun Venkatesan and Avindra Nath
Affiliation:
Keywords: HIV, AIDS, methamphetamine, brain, neuron, dopamine, Tat, gp120
Abstract: The use of methamphetamine is steadily increasing worldwide. Its use is associated with high-risk sexual behavior and subsequent infection with HIV. Methamphetamine has profound effects on the brain both as an acute intoxicant and following chronic exposure. The combined effects of HIV and methamphetamine appear to result in widespread neuronal and white matter injury. These changes are most prominent in the basal ganglia and frontal lobe, and are not restricted to dopaminergic neurons. Additionally, methamphetamine and HIV proteins disrupt the blood brain barrier, cause glial cell activation and impair the function of neural progenitor cells. Methamphetamine also results in increased HIV replication via activation of chemokine receptors involved in HIV entry. Common pathways in several of these effects seem to involve induction of oxidative stress. Characterization of these subcellular pathways and identification of common targets is essential for development of therapeutic strategies for HIV-infected methamphetamine abusers.
Export Options
About this article
Cite this article as:
Conant Katherine, Venkatesan Arun and Nath Avindra, Methamphetamine and HIV Infection, Role in Neurocognitive Dysfunction, Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry 2009; 8 (2) . https://dx.doi.org/10.2174/187152309789152084
DOI https://dx.doi.org/10.2174/187152309789152084 |
Print ISSN 1871-5230 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-614X |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Modulating Mitochondria-Mediated Apoptotic Cell Death through Targeting of Bcl-2 Family Proteins
Recent Patents on DNA & Gene Sequences Estrogen Receptor Neurobiology and its Potential for Translation into Broad Spectrum Therapeutics for CNS Disorders
Current Molecular Pharmacology Anaplastic Lymphoma Kinase as a Therapeutic Target in Anaplastic Large Cell Lymphoma, Non-Small Cell Lung Cancer and Neuroblastoma
Anti-Cancer Agents in Medicinal Chemistry Inhibition of Tau Aggregation in Cell Models of Tauopathy
Current Alzheimer Research Preventive and Protective Roles of Dietary Nrf2 Activators Against Central Nervous System Diseases
CNS & Neurological Disorders - Drug Targets Adjuvant Zoledronic Acid Reduces Disease Recurrence in Breast Cancer: Antitumor Effects on the Seed and the Soil
Current Cancer Therapy Reviews Intracellular Accumulation of Toxic Turn Amyloid-β is Associated with Endoplasmic Reticulum Stress in Alzheimer’s Disease
Current Alzheimer Research The Multiple Layers of Signaling Selectivity at Protease-Activated Receptors
Current Pharmaceutical Design Neuroprotective Therapies for Alzheimers Disease
Current Pharmaceutical Design Neuroprotective Role of Agmatine in Neurological Diseases
Current Neuropharmacology Small-Animal Molecular Imaging for Preclinical Cancer Research: μPET and μSPECT
Current Radiopharmaceuticals Multidrug-Resistance (MDR) Proteins Develops Refractory Epilepsy Phenotype:Clinical and Experimental Evidences
Current Drug Therapy Insights on the Structure of Amyloid Fibrils from Site-Directed Mutagenesis
Protein & Peptide Letters Therapeutic Strategies for Alzheimer's and Parkinson's Diseases by Means of Drug Delivery Systems
Current Medicinal Chemistry Neuroprotection by Resveratrol in Diabetic Neuropathy: Concepts & Mechanisms
Current Medicinal Chemistry A Second Look into the Oxidant Mechanisms in Alzheimers Disease
Current Neurovascular Research The Histone Deacetylase Inhibitor, MS-275 (Entinostat), Downregulates c-FLIP, Sensitizes Osteosarcoma Cells to FasL, and Induces the Regression of Osteosarcoma Lung Metastases
Current Cancer Drug Targets Anti-Cancer Drug Design Using Natural and Synthetic Pharmacophores
Current Organic Chemistry Bone Morphogenetic Protein-Smad Pathway as Drug Targets for Osteoporosis and Cancer Therapy
Endocrine, Metabolic & Immune Disorders - Drug Targets Carotenoids and Modulation of Cancer: Molecular Targets
Current Pharmacogenomics