Alpha EEG activity and subcortical pathology in HIV infection

Baldeweg, Torsten; Gruzelier, J.

doi:10.1016/s0167-8760(97)00780-0

Cited by 29 publications

(12 citation statements)

References 36 publications

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“…Schizophrenia [59], [60], [61], [62], depression and anxiety [60], [63], [64] and substance abuse disorders [65] can produce a similar change. The lack of GABAergic inhibitory control leads to heightened excitatory output from frontal neocortex [59], [62], which agrees with some electroencephalographic recordings made in patients with HIV/AIDS [66]. Regulation of neocortical GABAergic circuits in HAND may, therefore, reflect a generic change when frontal lobe output is abnormal.…”

Section: Discussionsupporting

confidence: 85%

The National NeuroAIDS Tissue Consortium Brain Gene Array: Two Types of HIV-Associated Neurocognitive Impairment

et al. 2012

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BackgroundThe National NeuroAIDS Tissue Consortium (NNTC) performed a brain gene expression array to elucidate pathophysiologies of Human Immunodeficiency Virus type 1 (HIV-1)-associated neurocognitive disorders.MethodsTwenty-four human subjects in four groups were examined A) Uninfected controls; B) HIV-1 infected subjects with no substantial neurocognitive impairment (NCI); C) Infected with substantial NCI without HIV encephalitis (HIVE); D) Infected with substantial NCI and HIVE. RNA from neocortex, white matter, and neostriatum was processed with the Affymetrix® array platform.ResultsWith HIVE the HIV-1 RNA load in brain tissue was three log10 units higher than other groups and over 1,900 gene probes were regulated. Interferon response genes (IFRGs), antigen presentation, complement components and CD163 antigen were strongly upregulated. In frontal neocortex downregulated neuronal pathways strongly dominated in HIVE, including GABA receptors, glutamate signaling, synaptic potentiation, axon guidance, clathrin-mediated endocytosis and 14-3-3 protein. Expression was completely different in neuropsychologically impaired subjects without HIVE. They had low brain HIV-1 loads, weak brain immune responses, lacked neuronally expressed changes in neocortex and exhibited upregulation of endothelial cell type transcripts. HIV-1-infected subjects with normal neuropsychological test results had upregulation of neuronal transcripts involved in synaptic transmission of neostriatal circuits.InterpretationTwo patterns of brain gene expression suggest that more than one pathophysiological process occurs in HIV-1-associated neurocognitive impairment. Expression in HIVE suggests that lowering brain HIV-1 replication might improve NCI, whereas NCI without HIVE may not respond in kind; array results suggest that modulation of transvascular signaling is a potentially promising approach. Striking brain regional differences highlighted the likely importance of circuit level disturbances in HIV/AIDS. In subjects without impairment regulation of genes that drive neostriatal synaptic plasticity reflects adaptation. The array provides an infusion of public resources including brain samples, clinicopathological data and correlative gene expression data for further exploration (http://www.nntc.org/gene-array-project).

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Section: Discussionsupporting

confidence: 85%

The National NeuroAIDS Tissue Consortium Brain Gene Array: Two Types of HIV-Associated Neurocognitive Impairment

et al. 2012

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“…Schizophrenia (Benes and Berretta, 2001; Markram et al, 2004; Hashimoto et al, 2008), depression and anxiety (Benes and Berretta, 2001; Sequeira et al, 2009; Sibille et al, 2011) and substance abuse disorders (Ke et al, 2004) have been shown to present similar changes in GABAergic function. The lack of GABAergic inhibitory control leads to heightened excitatory output from the frontal neocortex (Markram et al, 2004; Tepper et al, 2004), which agrees with some electroencephalographic recordings made in patients with HIV/AIDS (Baldeweg and Gruzelier, 1997). Further, a recent study using Tat transgenic mice indicated that HIV-1 Tat expression in the brain as well as acute Tat application in vitro generated a latent excitatory state, with increased stimulus-evoked glutamate exocytosis in the cortex and hippocampus while GABA exocytosis was decreased in the cortex (Zucchini et al, 2013).…”

Section: Discussionsupporting

confidence: 86%

Cannabinoids Occlude the HIV-1 Tat-Induced Decrease in GABAergic Neurotransmission in Prefrontal Cortex Slices

Hermes

Lichtman

et al. 2016

J Neuroimmune Pharmacol

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In the era of combined antiretroviral therapy (cART), human immunodeficiency virus type 1 (HIV-1) is now considered a chronic disease that specifically targets the brain and causes HIV-1-associated neurocognitive disorders (HAND). Endocannabinoids exhibit neuroprotective and anti-inflammatory properties in several central nervous system (CNS) disease models, but their effects in HAND are poorly understood. To address this issue, whole-cell recordings were performed on young (14 – 21 day old) C57BL/6J mice. We investigated the actions of the synthetic cannabinoid WIN55,212-2 (1 μM) and the endocannabinoid N-arachidonoyl ethanolamine (anandamide; AEA, 1 μM) in the presence of HIV-1 Tat on GABAergic neurotransmission in mouse prefrontal cortex (PFC) slices. We found a Tat concentration dependent (5 – 50 nM) decrease in the frequency and amplitude of miniature inhibitory postsynaptic currents (mIPSCs). The cannabinoid 1 receptor (CB1R) antagonist rimonabant (1 μM) and zero extracellular calcium prevented the significant Tat-induced decrease in mIPSCs. Further, bath-applied WIN55,212-2 or AEA by itself, significantly decreased the frequency, but not amplitude of mIPSCs and/or spontaneous IPSCs (sIPSCs), and occluded a further down-regulation of IPSCs by Tat. Pretreatment with rimonabant but not the CB2R antagonist AM630 (1 μM) prevented the WIN55,212-2- and AEA-induced decrease in IPSCs frequency without any further Tat effect. Results indicated a Tat-induced decrease in GABAergic neurotransmission, which was occluded by cannabinoids via a CB1R-related mechanism. Understanding the relationship between Tat toxicity and endocannabinoid signaling has the potential to identify novel therapeutic interventions to benefit individuals suffering from HAND and other cognitive impairments.

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“…The K v channel dysfunction may elucidate how abnormal electrical current output from brain cortex is produced in HAD, which can be recorded by electroencephalography (EEG) using scalp electrodes. It has been shown that an increase in the amplitude of α and θ waves of EEG can be recorded in HAD patients (Baldeweg and Gruzelier 1997;Polich et al 2000;Jeong et al 2001) and a left/bilateral temporooccipital focal slowing on EEG was described (Mehling et al 2008). As EEG wave oscillations originate from feedback loops between brain neocortex and subcortical regions such as the basal ganglia (Llinas et al 1999;Gelman et al 2004), the abnormal EEG recorded in HAD patients may reflect the underlying theory of the subcortical dementia (Gelman et al 2004).…”

Section: Abnormal Electroencephalography In Hadmentioning

confidence: 99%

Voltage-gated Potassium Channels in Human Immunodeficiency Virus Type-1 (HIV-1)-associated Neurocognitive Disorders

Keblesh

Xiong

2008

J Neuroimmune Pharmacol

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Human immunodeficiency virus type-1 (HIV-1)-associated dementia (HAD), a severe form of HIV-associated neurocognitive disorders (HAND), describes the cognitive impairments and behavioral disturbances which afflict many HIV-infected individuals. Although the precise mechanism leading to HAD is incompletely understood, it is commonly accepted its progression involves a critical mass of infected and activated mononuclear phagocytes (brain perivascular macrophages and microglia) releasing immune and viral products in the brain. These cellular and viral products induce neuronal dysfunction and injury via various signaling pathways. Emerging evidence indicates voltage-gated potassium (K v ) channels, key regulators of cell excitability and animal behavior (learning and memory), are involved in the pathogenesis of HAD/HAND. Here we survey the literature and find that HAD-related alterations in cellular and viral products can increase neuronal K v channel activity, leading to neuronal dysfunction and cognitive deficits. Thus, neuronal K v channels may be a new target in the effort to develop therapies for HAD and perhaps other inflammatory neurodegenerative disorders.

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Alpha EEG activity and subcortical pathology in HIV infection

Cited by 29 publications

References 36 publications

The National NeuroAIDS Tissue Consortium Brain Gene Array: Two Types of HIV-Associated Neurocognitive Impairment

The National NeuroAIDS Tissue Consortium Brain Gene Array: Two Types of HIV-Associated Neurocognitive Impairment

Cannabinoids Occlude the HIV-1 Tat-Induced Decrease in GABAergic Neurotransmission in Prefrontal Cortex Slices

Voltage-gated Potassium Channels in Human Immunodeficiency Virus Type-1 (HIV-1)-associated Neurocognitive Disorders

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