       Document 0449
 DOCN  M9620449
 TI    [HIV and dementia: neuropathology]
 DT    9602
 AU    Seilhean D; Duyckaerts C; Hauw JJ; Laboratoire de Neuropathologie R.
       Escourolle, Hopital de la; Salpetriere, Paris.
 SO    J Neuroradiol. 1995 Sep;22(3):161-2. Unique Identifier : AIDSLINE
       MED/96043309
 AB    Cognitive disorders associated with HIV infection may be due to focal
       lesions (lymphoma, toxoplasmosis, progressive multifocal
       leukoencephalitis, etc.), metabolic encephalopathy (e.g. hepatic
       insufficiency) or psychiatric disorders (depression). In the absence of
       such causes a cognitive and motor syndrome associated with HIV infection
       has been defined on clinical criteria (Working group of the American
       Academy of Neurology, 1991). This syndrome is not consistently
       associated with any specific lesion. Neither the multifocal encephalitis
       of HIV or CMV infection nor the diffuse leukoencephalopathy associated
       with HIV are the only causes. The existence of a neocortical neuronal
       loss has been suggested by several retrospective studies, but our
       prospective study has not shown cortical or subcortical atrophy.
       Measurement of neuronal density in Brodmann's areas 4,9 and 40 has not
       revealed a significant loss either global, by layer, or by column. The
       only constant lesion was gliosis of the cortex and white matter.
       Neuronal loss, therefore, is not indispensable to the occurrence of
       cognitive disorders in AIDS. The mechanism of dementia might be:
       dysfunction of cortical neurons (dendritic abnormalities,
       virus/neurotransmitter competition); subcortical dysfunction, as
       suggested by the high density of microglial nodules in that region;
       white matter lesions which could be due to abnormalities in the
       blood-brain barrier. The expression of cell adhesion molecules (VCAM-1,
       VLA-4, ICAM-1 and LFA-1) by endothelial cerebral cells is not
       significantly different in AIDS patients, demented or not, and in
       patients with multiple sclerosis. In contrast, the expression of VCAM-1
       by astrocytes is significantly increased in demented AIDS patients
       compared with non demented ones.(ABSTRACT TRUNCATED AT 250 WORDS)
 DE    Atrophy  AIDS Dementia Complex/GENETICS/METABOLISM/*PATHOLOGY/PSYCHOLOGY
       Blood-Brain Barrier  Cell Adhesion Molecules/GENETICS  Cerebral
       Cortex/PATHOLOGY  Comparative Study  Cytomegalovirus
       Infections/PATHOLOGY  Encephalitis, Viral/PATHOLOGY  English Abstract
       Gene Expression  Gliosis/PATHOLOGY  Human  HIV Infections/PATHOLOGY
       Leukoencephalopathy, Progressive Multifocal/PATHOLOGY
       Microglia/PATHOLOGY  Multiple Sclerosis/GENETICS/METABOLISM
       Neurons/PATHOLOGY  Prospective Studies  Retrospective Studies  JOURNAL
       ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

