AIDS dementia complex with generalized myoclonus

Maher, John; Choudhri, S. H.; Halliday, William; Power, Christopher; Nath, Avindra

doi:10.1002/mds.870120418

Cited by 36 publications

(11 citation statements)

References 17 publications

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“…The brain pathology shows neuronal damage and death (Kolson 2002). HIV-1-associated dementia (HAD) is characterized by progressive cognitive impairment and motor dysfunction (Maher et al 1997). The incidence is about 14% within 2 years after AIDS onset ( McArthur et al 1993).…”

Section: Retroviral Neuropathogenesismentioning

confidence: 99%

HERVs in Neuropathogenesis

Christensen

2010

J Neuroimmune Pharmacol

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In humans, exogenous retroviruses are known to cause immunodeficiency and neurological disease. While endogenous retroviruses are firmly established pathogens in other species, the human endogenous retroviruses (HERVs) may well be considered as emerging pathogens. HERVs also exhibit complex interactions with exogenous retroviruses and herpesviruses. Two neurological disorders in particular are associated with HERVs: multiple sclerosis (MS) and schizophrenia. HERV-H/F and HERV-W are specifically activated both in the circulation and the central nervous system (CNS) in a majority of MS patients, and particularly, the envelopes (env transcription and Env proteins) appear strongly associated with disease activity. Interferon beta (IFN-beta) therapy is well-established for MS. IFN-beta is also known to have anti-retroviral activities toward exogenous retroviruses (HIV and HTLV-I). New reports show that IFN-beta also mediate down-regulation of HERV-H/F and HERV-W in MS patients. HERV-W and HERV-K transcription (gag and pol) appears, to some extent, to be up-regulated in the circulation and the CNS of patients with schizophrenia. The expression of anti-HERV-W Gag reactive epitopes is reported to be down-regulated in the brain but up-regulated in the blood from schizophrenia patients. The pathogenic potential of HERVs certainly merits further studies.

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Section: Retroviral Neuropathogenesismentioning

confidence: 99%

HERVs in Neuropathogenesis

Christensen

2010

J Neuroimmune Pharmacol

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“…Generalized chorea may occur as a result of bilateral abscesses of toxoplasmosis (Gallo et al, 1996). Myoclonus, is generalized and elicited by sudden auditory stimuli that resembles a startled response, has also been described in AIDS-associated CT patients (Maher et al, 1997). A case of focal dystonia of the left arm and hand has been reported in an AIDS patient due to the right lenticular nucleus and thalamic abscesses of toxoplasmosis (Tolge & Factor, 1991).…”

Section: Cerebral Toxoplasmosismentioning

confidence: 99%

Toxoplasmosis in HIV/AIDS Patients - A Living Legacy

Nissapatorn¹

2011

Microbes, Viruses and Parasites in AIDS Process

101

124

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“…In the absence of identifiable opportunistic infections, patients might present with the AIDS dementia complex, also called HIV-associated dementia (HAD), HIV dementia or HIV encephalopathy, which is characterized by deficits in attention, impairments of short-term memory, compromised fine motor skills, tremors, slowness of movements and abnormal gait (Navia et al, 1986b;Power and Johnson, 1995). Some develop seizures and myoclonic jerks (Maher et al, 1997). Over periods of weeks to months, patients can become very demented, quadriparetic, and incontinent (Navia et al, 1986b).…”

Section: Neuropsychiatry Neuroimaging and Neuropathology Of Eiiv Infecmentioning

confidence: 99%

Interactions of HIV and methamphetamine: Cellular and molecular mechanisms of toxicity potentiation

Cadet

Krasnova

2007

neurotox res

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Methamphetamine (METH) is a highly addictive psychostimulant drug, whose abuse has reached epidemic proportions worldwide. METH use is disproportionally represented among populations at high risks for developing HIV infection or who are already infected with the virus. Psychostimulant abuse has been reported to exacerbate the cognitive deficits and neurodegenerative abnormalities observed in HIV-positive patients. Thus, the purpose of the present paper is to review the clinical and basic observations that METH potentiates the adverse effects of HIV infection. An additional purpose is to provide a synthesis of the cellular and molecular mechanisms that might be responsible for the increased toxicity observed in co-morbid patients. The reviewed data indicate that METH and HIV proteins, including gp120, gp41, Tat, Vpr and Nef, converge on various caspase-dependent death pathways to cause neuronal apoptosis. The role of reactive microgliosis in METH- and in HIV-induced toxicity is also discussed.

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AIDS dementia complex with generalized myoclonus

Cited by 36 publications

References 17 publications

HERVs in Neuropathogenesis

HERVs in Neuropathogenesis

Toxoplasmosis in HIV/AIDS Patients - A Living Legacy

Interactions of HIV and methamphetamine: Cellular and molecular mechanisms of toxicity potentiation

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