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We are analyzing https://link.springer.com/article/10.1007/s11481-006-9018-2.

Title:
Neurobiology of Multiple Insults: HIV-1-Associated Brain Disorders in Those Who Use Illicit Drugs | Journal of Neuroimmune Pharmacology
Description:
Despite two decades of research, certain aspects of HIV-related central nervous system (CNS) disease remain poorly understood. HIV targets microglia and macrophages within the CNS and enters the brain compartment early. However, HIV is there held in check apparently until the onset of significant immune compromise, when viral replication, microglial activation, neuronal damage, and cognitive impairment are likely to ensue. Illicit drug abuse continues to be a significant risk factor for HIV transmission worldwide. Whether HIV-related CNS disease is more prevalent or more severe in this risk group has long been debated. Drugs of abuse can of themselves cause immune suppression, blood–brain barrier breakdown, microglial activation, and neuronal injury. This review presents evidence that HIV associated CNS disorders are indeed accentuated in drug abusers. However, the advent of effective therapy has added a new dimension, which must be taken into consideration. Treated individuals are surviving much longer and HIV encephalitis and HIV-associated dementia have become much less common. However, more subtle forms of CNS damage are emerging. Examination of the brains of individuals who have been treated long term with highly active antiretroviral therapy (HAART) reveals a surprising degree of microglial activation, comparable at times to that seen formerly in milder cases of HIV encephalitis. In addition, these individuals show evidence of increased deposition of neurodegenerative proteins, particularly hyperphosphorylated tau. Similar observations have been made in young opiate abusers who are HIV negative. Taken together, these results suggest that neuroinflammation and neurodegeneration, which are clinically silent at present, may cause problems in the future in HAART-treated subjects.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We don’t know how the website earns money.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

Keywords {🔍}

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Topics {✒️}

month download article/chapter immune-competent mononuclear phagocytes antibody-positive virus carrier juan-carlos arango & iain hiv-seropositive homosexual men asymptomatic hiv-positive patients hiv-infected drug addicts blood–brain barrier breakdown acquired immunodeficiency syndrome pre-symptomatic hiv infection human immunodeficiency virus human immunodeficiency virus full article pdf hepatic encephalopathy hiv-related cns disease privacy choices/manage cookies central nervous system metabolic encephalopathy perpetrated sharer lr significant immune compromise neuroimmune pharmacology aims hiv-related studies human brain tissue anti-retroviral therapy endogenous opioid system csf amyloid beta42 review presents evidence anthony ic pre-aids subjects haart-treated subjects significant risk factor hiv-1 infections early hiv-1 infection magnetic resonance study electron microscopical study comparative international study torres-munoz serotonin transporter gene multinucleated giant cells hippocampal neurons isolated laser capture microdissection alexander donald building western general hospital blood–brain barrier article journal young drug abusers conditions privacy policy injection drug users hiv cellular reservoirs hiv-1 gene sequences

Questions {❓}

  • Cocaine's connection to AIDS dementia and vasculitis?
  • Tyor W, Middaugh LD (1999) Do alcohol and cocaine abuse alter the course of the HIV-associated dementia complex?

Schema {🗺️}

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         headline:Neurobiology of Multiple Insults: HIV-1-Associated Brain Disorders in Those Who Use Illicit Drugs
         description:Despite two decades of research, certain aspects of HIV-related central nervous system (CNS) disease remain poorly understood. HIV targets microglia and macrophages within the CNS and enters the brain compartment early. However, HIV is there held in check apparently until the onset of significant immune compromise, when viral replication, microglial activation, neuronal damage, and cognitive impairment are likely to ensue. Illicit drug abuse continues to be a significant risk factor for HIV transmission worldwide. Whether HIV-related CNS disease is more prevalent or more severe in this risk group has long been debated. Drugs of abuse can of themselves cause immune suppression, blood–brain barrier breakdown, microglial activation, and neuronal injury. This review presents evidence that HIV associated CNS disorders are indeed accentuated in drug abusers. However, the advent of effective therapy has added a new dimension, which must be taken into consideration. Treated individuals are surviving much longer and HIV encephalitis and HIV-associated dementia have become much less common. However, more subtle forms of CNS damage are emerging. Examination of the brains of individuals who have been treated long term with highly active antiretroviral therapy (HAART) reveals a surprising degree of microglial activation, comparable at times to that seen formerly in milder cases of HIV encephalitis. In addition, these individuals show evidence of increased deposition of neurodegenerative proteins, particularly hyperphosphorylated tau. Similar observations have been made in young opiate abusers who are HIV negative. Taken together, these results suggest that neuroinflammation and neurodegeneration, which are clinically silent at present, may cause problems in the future in HAART-treated subjects.
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      headline:Neurobiology of Multiple Insults: HIV-1-Associated Brain Disorders in Those Who Use Illicit Drugs
      description:Despite two decades of research, certain aspects of HIV-related central nervous system (CNS) disease remain poorly understood. HIV targets microglia and macrophages within the CNS and enters the brain compartment early. However, HIV is there held in check apparently until the onset of significant immune compromise, when viral replication, microglial activation, neuronal damage, and cognitive impairment are likely to ensue. Illicit drug abuse continues to be a significant risk factor for HIV transmission worldwide. Whether HIV-related CNS disease is more prevalent or more severe in this risk group has long been debated. Drugs of abuse can of themselves cause immune suppression, blood–brain barrier breakdown, microglial activation, and neuronal injury. This review presents evidence that HIV associated CNS disorders are indeed accentuated in drug abusers. However, the advent of effective therapy has added a new dimension, which must be taken into consideration. Treated individuals are surviving much longer and HIV encephalitis and HIV-associated dementia have become much less common. However, more subtle forms of CNS damage are emerging. Examination of the brains of individuals who have been treated long term with highly active antiretroviral therapy (HAART) reveals a surprising degree of microglial activation, comparable at times to that seen formerly in milder cases of HIV encephalitis. In addition, these individuals show evidence of increased deposition of neurodegenerative proteins, particularly hyperphosphorylated tau. Similar observations have been made in young opiate abusers who are HIV negative. Taken together, these results suggest that neuroinflammation and neurodegeneration, which are clinically silent at present, may cause problems in the future in HAART-treated subjects.
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