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Titolo:
A NEURONAL AND NEUROANATOMICAL CORRELATE OF HIV-1 ENCEPHALOPATHY RELATIVE TO HIV-1 ENCEPHALITIS IN HIV-1-INFECTED CHILDREN
Autore:
DACUNHA A; MINTZ M; EIDEN LE; SHARER LR;
Indirizzi:
GEORGETOWN UNIV,DEPT BIOL,POB 30166 BETHESDA MD 20824 NIMH,CELL BIOL LAB,NIH BETHESDA MD 20892 UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DIV PEDIAT NEUROL CAMDEN NJ 08103 UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT LAB MED & PATHOL,DIV NEUROPATHOL NEWARK NJ 07103
Titolo Testata:
Journal of neuropathology and experimental neurology
fascicolo: 9, volume: 56, anno: 1997,
pagine: 974 - 987
SICI:
0022-3069(1997)56:9<974:ANANCO>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-IMMUNODEFICIENCY-VIRUS; IMMUNE-DEFICIENCY-SYNDROME; CENTRAL-NERVOUS-SYSTEM; AIDS DEMENTIA COMPLEX; TUMOR-NECROSIS-FACTOR; PROGRESSIVE ENCEPHALOPATHY; CEREBRAL-CORTEX; MESSENGER-RNA; HUMAN-BRAIN; NEUROLOGIC MANIFESTATIONS;
Keywords:
AIDS; CHILDREN; ENCEPHALITIS; ENCEPHALOPATHY; MESSENGER-RNA; SIV; SOMATOSTATIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
74
Recensione:
Indirizzi per estratti:
Citazione:
A. Dacunha et al., "A NEURONAL AND NEUROANATOMICAL CORRELATE OF HIV-1 ENCEPHALOPATHY RELATIVE TO HIV-1 ENCEPHALITIS IN HIV-1-INFECTED CHILDREN", Journal of neuropathology and experimental neurology, 56(9), 1997, pp. 974-987

Abstract

Progressive central nervous system dysfunction analogous to the AIDS dementia complex (ADC) seen in adults (HIV-1-associated progressive encephalopathy or HIV-1 encephalopathy) commonly occurs in HIV-1-infected children. The cause appears to be directly or indirectly related to HIV-1, rather than to other opportunistic pathogens. The exact mechanism(s) by which the virus affects brain function is not known. To determine whether the virus might modify brain function via an alteration in cortical neurons, we examined peptide neurotransmitter expression inthe frontal cortex of HIV-1-infected cases with clinical HIV-1 encephalopathy relative to pathologic HIV-1 encephalitis. In situ hybridization was used to determine the level of peptide neurotransmitter expression of somatostatin in the frontal cortex of cases with and without HIV-1 encephalopathy and/or HIV-1 encephalitis. A 2-fold higher number of preprosomatostatin mRNA-positive interneurons was present in layer IV of cases with HIV-1 encephalitis compared with cases without HIV-1 encephalitis. In cases with PE, this neuronal alteration was 4- to 5-fold higher than in cases without PE, and was present in subcortical white matter in addition to layer IV. In cases having both PE and HIV-1 encephalitis, and in cases with HIV-1 encephalitis alone, these neuronal alterations in layer TV and/or subcortical white matter related to disseminated microglial nodules, even when these potentially viral-infected cells were negative for HIV-1 p24 antigen, a marker of productive viral infection. An alteration in preprosomatostatin mRNA-expressingcells occurring with HIV-1 encephalitis may be at least one mechanismthat contributes to HIV-1 encephalopathy. When compared with other cortical laminae, layer IV receives most of its synaptic input from the mediodorsal nucleus of the thalamus. Neurons in the subcortical white matter project to the thalamus. The thalamus has been shown to have high amounts of viral antigen and increased metabolic activity in patients with AIDS. An alteration in preprosomatostatin mRNA-expressing cells may play a role in HIV-1 encephalopathy.

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Documento generato il 02/12/20 alle ore 17:47:12