Gene expression profile in rat dorsal root ganglion following sciatic nerve injury and systemic neurotrophin-3 administration.

Following sciatic nerve transection in adult rats, a proportion of injured dorsal root ganglion (DRG) neurons die, through apoptosis, over the following 6 months. Previous studies showed that axotomy and neurotrophin-3 administration may have effects on expression of neurotrophins and their receptors in DRG. In the current study, the fourth and fifth lumbar DRGs of rats were examined 2 weeks after right sciatic nerve transection and ligation.

Effects of formalin fixation on magnetic resonance indices in multiple sclerosis cortical gray matter.

Purpose: To investigate changes in magnetic resonance imaging (MRI) indices following formalin fixation of postmortem multiple sclerosis (MS) cortical gray matter (CGM). Postmortem MS brain is being used to establish pathological correlates of changes detected using MRI, with recent emphasis on CGM. Fixation induces tissue alterations that may confound inference of in vivo observations from MRI/histology correlation studies.

High field (9.4 Tesla) magnetic resonance imaging of cortical grey matter lesions in multiple sclerosis.

Multiple sclerosis is an inflammatory, degenerative disease of the central nervous system. The most obvious pathological change in multiple sclerosis is multifocal demyelination of the white matter, but grey matter demyelination may be of equal or even greater importance for its clinical manifestations. In order to assess the pathogenetic role of lesions in the grey and white matter, and to explore the association between demyelinated and non-lesional brain tissue, tools are needed to depict each of these tissue components accurately in vivo.

Accumulation of prion protein in the peripheral nervous system in human prion diseases.

After the finding that anti-prion antibodies stain sensory and sympathetic ganglia in variant Creutzfeldt-Jakob disease (vCJD), it was suggested that this localization supported the oral route of entry. However, prion accumulation subsequently also appeared in the peripheral nervous system (PNS) in sporadic cases. This study aims at evaluating the extent of prion protein accumulation in the PNS in all clinicopathologic subgroups of the disorder, with the exception of the familial and sporadic forms of fatal insomnia.

Cerebral CD8+ lymphocytosis in HIV-1 infected patients with immune restoration induced by HAART.

In HIV infected persons, highly active antiretroviral therapy (HAART) has reduced both the morbidity and incidence of several disorders. Its effects on direct HIV-induced damage to the CNS remain controversial. In addition, HAART may provoke an "immune reconstitution inflammatory syndrome" (IRIS).

Detection of infectious agents in brain of patients with acute hemorrhagic leukoencephalitis.

Acute hemorrhagic leukoencephalitis (AHL) is a rare and usually fatal disorder characterized clinically by an acute onset of neurologic abnormalities. It may occur in association with a viral illness or vaccination. Radiology and brain biopsy are essential for the diagnosis.

The pathology of the spinal cord in progressive supranuclear palsy.

We describe the results of a study of the spinal cord of 5 patients with progressive supranuclear palsy (PSP). Examination of the 6th cervical, 7th thoracic, and 5th lumbar segments revealed variable degree of gliosis and density of neuropil threads (NTs), nerve cell loss, and tau-positive cytoplasmic staining of neurons, some of which was reminiscent of neurofibrillary tangles (NFT). Tau-positive neurons were seen at each spinal level and in the 3 zones in which each level was subdivided.

Neuronal intranuclear inclusions in SCA2: a genetic, morphological and immunohistochemical study of two cases.

Spinocerebellar ataxia 2 (SCA2) belongs to the family of autosomal dominant cerebellar ataxias (ADCA), a genetically heterogeneous group of neurodegenerative diseases. The SCA2 gene maps to chromosome 12q24 and the causative mutation involves the expansion of a CAG repeat within the coding region of the gene. Pathologically, SCA2 presents as olivo-ponto-cerebellar atrophy (OPCA).