Cerebrospinal fluid catecholamine metabolites in HIV‐infected patients

Larsson, Maria; Hagberg, Lars; Forsman, Anders; Norkrans, Gunnar

doi:10.1002/jnr.490280313

Cited by 70 publications

(36 citation statements)

References 12 publications

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“…CSF levels of dopamine in HIV-1-positive individuals without neurological disease were on average approximately 60% less than in seronegative controls, and those seropositive individuals with evidence of neurological disease on average had 80% less dopamine in CSF. In addition, decreased levels of HVA have also been reported in the CSF of HIV-infected patients [33,34]. Importantly, Larsson et al [33] observed the decrease only during the AIDS stage.…”

Section: Hiv/aids and Dopamine Levelsmentioning

confidence: 85%

“…In addition, decreased levels of HVA have also been reported in the CSF of HIV-infected patients [33,34]. Importantly, Larsson et al [33] observed the decrease only during the AIDS stage. Obermann at al [35] went further using transcranial sonographic (TCS) examination to assess the morphology of the substantia nigra, a region rich in dopaminergic cell bodies, and its relationship to dopamine levels in the CSF, and with neuropsychological performance in different stages of HIV infection.…”

Section: Hiv/aids and Dopamine Levelsmentioning

confidence: 85%

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Drugs of Abuse, Dopamine, and HIV-Associated Neurocognitive Disorders/HIV-Associated Dementia

Purohit

Rapaka²,

Shurtleff³

2011

Mol Neurobiol

110

104

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Section: Hiv/aids and Dopamine Levelsmentioning

confidence: 85%

Section: Hiv/aids and Dopamine Levelsmentioning

confidence: 85%

Drugs of Abuse, Dopamine, and HIV-Associated Neurocognitive Disorders/HIV-Associated Dementia

Purohit

Rapaka²,

Shurtleff³

2011

Mol Neurobiol

110

104

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“…Since deficits in neurological and neurocognitive functions found in HIV-1 infected patients were similar to those found in patients with Parkinson's disease (PD), such as bradykinesia, postural instability and their striking sensitivity to dopamine blocking agents, such as metoclopropamide, or chlorpromazine [17] , it was conceptualized that central dopamine deficiency may occur in HIV-1 infection. The support for this concept was provided by the studies carried out by our group and by others showing a decrease in the levels of dopamine, as well as HVA, in the CSF of patients who were infected with HIV-1 [18,11] . Since, the relationship between the decreased levels of dopamine in the CNS and cognitive dysfunctions caused by HIV-1 are not clearly understood, we investigated the status of dopamine in different regions of post mortem brains of HIV-1 infected patients who were assessed for cognitive performance during life.…”

Section: Introductionmentioning

confidence: 80%

HIV-1 Infection and Central Monoamine Neurotransmitters

Kumar¹,

Fernandez²,

Borodowsky³

et al. 2007

American J. of Infectious Diseases

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Human immunodeficiency virus type 1 (HIV-1) enters the central nervous system (CNS) shortly after infection and gets localized in different brain regions, leading to various types of neuropathological problems. It has been hypothesized that HIV-1 infection mediated neuropathogenesis may also adversely affect the activity of the central monoamine neurotransmitters systems, such as dopamine (DA), and 5-hydroxytryptamine (5-HT, serotonin), resulting in neurocognitive deficits and mental health problems. However, investigations are scarce with respect to the status of these neurotransmitters in the CNS of HIV-1+ individuals, particularly in those patients who had received antiretroviral therapy (ART) during life. Since, mental health problems and neurocognitive and neuropsychological deficits continue to persist even after ART intervention, it is pertinent to determine the CNS status of the neurotransmitters associated with these functions. We determined the neurotransmitters, dopamine and its metabolite, homovanillic acid (HVA) in different brain regions of a group of autopsied cases of HIV-1+ and HIV-1 negative controls, using highly sensitive CoulArray HPLC-ECD system. Distribution of HIV-1 viral RNA in these brain regions was also measured using real-time reverse transcriptase polymerase chain reaction (real-time RT-PCR) technology with high sensitivity of detection (<5 copies of RNA). In a separate study we reported measurement of 5-HT (serotonin) and its metabolite, 5-hydroxyindole acetic acid (5-HIAA) in the cerebrospinal fluid (CSF) obtained during life of neurologically asymptomatic HIV-1 infected patients and controls. A substantial decrease and a wide variation in the concentration of DA as well as its metabolite, homovanillic acid (HVA) was found in the autopsied brain regions of HIV-1 infected individuals. Wide variation was also found in HIV-1 RNA concentrations in different brain regions with no specific pattern observed in any region. Brain regions of HIV-negative individuals showed no detectable viral RNA. Majority of HIV-1+ individuals had demonstrated neurocognitive impairment during life despite ART intervention. A significant decrease in 5-HT concentration was also found in the CSF of HIV-1 infected patients. These studies demonstrate that HIV-1 infection adversely affects the central DA and 5-HT systems.

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“…Deficits in CSF levels of dopamine and its metabolites have been measured in HIV-1-infected patients (Larsson et al 1991;Berger et al 1994;di Rocco et al 2000). Moreover, signs of parkinsonism including bradykinesia, postural instability and gait disturbances and sensitivity to parkinsonian-inducing agents, have been reported in patients infected with HIV-1 (For review see Berger and Nath 1997).…”

Section: Discussionmentioning

confidence: 99%

Human immunodeficiency virus‐1 Tat protein and methamphetamine interact synergistically to impair striatal dopaminergic function

Maragos¹,

Young²,

Turchan³

et al. 2002

Journal of Neurochemistry

115

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The human immunodeficiency virus (HIV)-1 transactivating protein Tat may be pathogenically relevant in HIV-1-induced neuronal injury. The abuse of methamphetamine (MA), which is associated with behaviors that may transmit HIV-1, may damage dopaminergic afferents to the striatum. Since Tat and MA share common mechanisms of injury, we examined whether co-exposure to these toxins would lead to enhanced dopaminergic toxicity. Animals were treated with either saline, a threshold dose of MA, a threshold concentration of Tat injected directly into the striatum, or striatal injections of Tat followed by exposure to MA. Threshold was defined as the highest concentration of toxin that would not result in a significant loss of striatal dopamine levels. One week later, MA-treated animals demonstrated a 7% decline in striatal dopamine levels while Tat-treated animals showed an 8% reduction. Exposure to both MA + Tat caused an almost 65% reduction in striatal dopamine. This same treatment caused a 56% reduction in the binding capacity to the dopamine transporter. Using human fetal neurons, enhanced toxicity was also observed when cells were exposed to both Tat and MA. Mitochondrial membrane potential was disrupted and could be prevented by treatment with antioxidants. This study demonstrates that the HIV-1 ÔvirotoxinÕ Tat enhances MAinduced striatal damage and suggests that HIV-1-infected individuals who abuse MA may be at increased risk of basal ganglia dysfunction.

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Cerebrospinal fluid catecholamine metabolites in HIV‐infected patients

Cited by 70 publications

References 12 publications

Drugs of Abuse, Dopamine, and HIV-Associated Neurocognitive Disorders/HIV-Associated Dementia

Drugs of Abuse, Dopamine, and HIV-Associated Neurocognitive Disorders/HIV-Associated Dementia

HIV-1 Infection and Central Monoamine Neurotransmitters

Human immunodeficiency virus‐1 Tat protein and methamphetamine interact synergistically to impair striatal dopaminergic function

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