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P Mehraein

Publications and source records attributed to P Mehraein.

At least 37 records · Page 2Linked to original sources
PubMed1996

Vascular changes in the cerebral cortex in HIV-1 infection. II. An immunohistochemical and lectinhistochemical investigation.

In human immunodeficiency virus 1 (HIV-1)-infected patients, a hypoperfusion is seen by SPECT analyses in different brain regions but a specific pattern for the predominance of a specific brain region has not been found. The vessels of the cerebral cortex of the frontal, temporal, parietal, and occipital lobes of acquired immunodeficiency syndrome (AIDS) brains and control brains were analyzed by immunohistochemistry and lectin histochemistry. Immunohistochemistry was performed for collagen IV, laminin (basal lamina), and factor VIII (endothelial cell) and lectin histochemistry [Ricinus communis agglutinin (RCA-I), Ulex europaeus agglutinin (UEA-I), wheatgerm agglutinin (WGA) and soybean agglutinin (SBA)] was used to study changes of glycoproteins in the endothelial cell membrane. Vessels were counted in the gray and white matter, and their staining intensity for the different antibodies and lectins was rated using a three-point scale. Immunoreactivity for collagen IV was reduced in AIDS brains, which may be related to thinning of the basal lamina of cerebral vessels, as has previously been shown by electron microscopy. Lectin histochemistry with SBA, UEA-I and WGA indicated loss of glycoproteins in the membrane of endothelial cells. The data from the present study show morphological changes of the endothelial cells and of the basal lamina in the brain of individuals with AIDS, and might represent the morphological sequelae of a disturbed blood-brain barrier, or may account for the hypoperfusion seen in SPECT analyses.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Degeneration of the cerebellar dentate nucleus and the inferior olivary nuclei in HIV-1-infected brains: a morphometric analysis.

Motor dysfunction is frequently noted in human immunodeficiency virus type 1 (HIV-1)-infected patients. Until recently, neuropathological changes found in the basal ganglia were advanced as pathogenetic mechanisms. In the present study, further brain structures involved in motor control were analyzed morphometrically. The volume density, numerical density, and the size of neurons in the cerebellar dentate nucleus and in both inferior olivary nuclei were determined. In both regions of HIV-1-infected brains, a significant reduction in the volume density, the numerical density of neurons and neuronal size was apparent. The morphometric data from the present study disclose involvement of both types of nuclei investigated during the course of HIV-1 infection, and might constitute a possible morphological substrate for the motor dysfunction seen in HIV-1-infected patients.

Adult↗
PubMed1996

Signal changes on MRI and increases in reactive microgliosis, astrogliosis, and iron in the putamen of two patients with multiple system atrophy.

A correlation of clinical, MRI, and neuropathological data is reported in two patients with multiple system atrophy (MSA). On MRI, patient 1 showed striatal atrophy, reduction of T2 relaxation times within most of the putamen, and a band of hyperintense signal changes in the lateral putamen. In patient 2, MRI disclosed only shortening of the T2 signal in the putamen. Immunohistochemistry showed pronounced reactive microgliosis and astrogliosis in the affected brain regions. In patient 1, the area with the most pronounced microgliosis and astrogliosis most likely correlated with the area of hyperintense signal changes on MRI. This area also contained the highest amount of ferric iron, which was increased in the putamen of patient 1 but not patient 2. It is unlikely that the hypointense signal changes in the putamen are due to an increase of iron alone. Reactive microglial and astroglial cells may play a part in the pathogenesis of MSA.

Adult↗
PubMed1996

CMV-infected subependymoma in the fourth ventricle of an HIV-1 infected patient.

A case of an AIDS patient with a CMV-infected subependymoma of the fourth ventricle is presented. The tumor was incidentally found at autopsy and was not suspected during the clinical course. This is the first report of a subependymoma in HIV-1 infection. Moreover, infection of a tumor with CMV is an extremely rare condition, which has until now been described only once in an anaplastic astrocytoma.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Absence of the mitochondrial A7237T mutation in Parkinson's disease.

In recent years much has been speculated about a pathogenic role of mitochondrial defects in Parkinson's disease. Ozawa et al. (BBRC 176, 938-946, 1991) have described an A/T transversion at nucleotide 7237 of mitochondrial DNA affecting cytochrome-c-oxidase (complex IV) of the respiratory chain that could contribute to the pathogenesis of PD. Employing PCR based genomic sequencing and restriction enzyme analysis on 19 cases of Lewy-body parkinsonism, we exclude this mutation as a common cause of Parkinson's disease. This demonstrates the need for systematic sequencing of the mitochondrial genome in a large number of histologically verified cases of Parkinson's disease.

Adenine↗
PubMed1995

Apolipoprotein E genotype and neuropathological phenotype in two members of a German family with chromosome 14-linked early onset Alzheimer's disease.

Molecular genetic analysis was performed in two autopsy-confirmed cases of early-onset Alzheimer's disease belonging to a large German pedigree [FAD2, according to the nomenclature of St. George-Hyslop, et al. (1987) Science 235:885-890]. The disease in this family has been linked to chromosome 14. As gene interactions are considered to influence the age of onset and tissue pathology in Alzheimer's disease, we have studied three candidate genes that could modify disease progression. In this study a new polymerase chain reaction (PCR) assay was established for apolipoprotein E genotyping in archival neuropathological tissue, exon 17 of the amyloid precursor protein gene was directly sequenced, and a candidate mutation site at nucleotide (nt) 5460 of the mitochondrial NADH dehydrogenase subunit gene ND2 was analyzed employing PCR followed by HphI digestion. Whereas no sequence variations were detected in exon 17APP or at nt5460 of mitochondrial DNA, the apolipoprotein E genotypes of the two cases differed. Neuropathological examination revealed a higher number of beta A4-positive amyloid plaques and a larger total tissue area covered by beta A4 deposits in the epsilon 3/epsilon 3 homozygote. In contrast, the number of cortical neurofibrillary tangles and the number of plaques with tau-positive neurites appeared to be higher in the epsilon 3/epsilon 4 heterozygote. Our findings support the view that the chromosome 14 genetic defect, rather than apolipoprotein E genotype, is the preeminent factor determining Alzheimer's disease pathology in this family.

Alzheimer Disease↗
PubMed1994

No association of mutations at nucleotide 5460 of mitochondrial NADH dehydrogenase with Alzheimer's disease.

NADH dehydrogenase (EC 1.6.99.3) mutations at nucleotide 5460 of mitochondrial DNA (codon 331 of the ND2 subunit gene) have been associated with Alzheimer's disease (BBRC 182, 238-246, 1992; BBRC 189, 1202-1206, 1992). We have sequenced codons 304-347 of this gene in 15 neuropathologically confirmed cases of Alzheimer's disease. In addition, restriction enzyme analysis was performed on the same cases and on 28 control brains. No mutations were detected in the Alzheimer brains but heteroplasmy for a G-->A transition at nucleotide 5460 of mtDNA was found in the frontal cortex of a single control. Thus, our findings do not confirm reports of a significant association between mutations at nucleotide 5460 of mitochondrial DNA and Alzheimer's disease.

Aged↗
PubMed1994

Activation of microglia in HIV-1 infected brains is not dependent on the presence of HIV-1 antigens.

The activation pattern of microglia in the cerebral cortex of AIDS patients with the neuropathological diagnosis of HIV-1 encephalitis was investigated by immunohistochemistry and morphometry. The number of activated microglial cells in the grey and white matter of five cortical regions was determined. In the grey and white matter of all cortical regions a significant increase in the number of microglial cells was demonstrated in HIV-1 infected brains. Moreover, the activation of microglia was not correlated with the presence of HIV-1 antigen in the brain region. The data show a significantly increased number of microglia in HIV-1 infected brains. These activated microglial cells could, among others, be those cells producing cytotoxic factors which, in turn, cause brain damage.

AIDS Dementia Complex↗
PubMed1994

Distribution of prion protein in German patients with Creutzfeldt-Jakob disease is different from that in Japanese patients.

We investigated the distribution of prion protein (PrP) in 14 German patients with sporadic Creutzfeldt-Jakob disease (CJD) and compared it with that observed in Japanese patients. Immunohistochemical study revealed diffuse gray matter stainings including synaptic structures in all cases. In addition, 4 patients showed plaque-type deposition which was very rarely observed among sporadic Japanese patients without known mutation of the PrP gene but with valine at codon 129. A higher incidence of PrP plaques in German sporadic CJD may be related to the racial difference in the PrP gene.

Adult↗
PubMed1994

A modified NOR-silver impregnation technique for amyloid plaques and neurofibrillary tangles: comparative assessment.

A modified nucleolar organizer region (NOR)-silver impregnation technique was recently introduced allowing the simultaneous staining of neurofibrillary tangles (NFT) and amyloid plaques (AP) in a single section. This impregnation technique proved to be very effective, rapid, of low cost, and to yield consistent results even in brain tissue fixed for long periods of time. In the present study, several silver impregnation and immunohistochemical techniques were applied and their reliability for the demonstration of NFT and AP was analysed. The modified NOR stain allowed the reliable and simultaneous demonstration of both amyloid plaques and neurofibrillary tangles; this method produced better results than the standard silver impregnation techniques. It is only in their early stages of formation that NFT cannot be detected by this method and, instead, immunohistochemistry for tau-2 is required. There was no significant difference in the staining properties for amyloid plaques between the modified NOR silver impregnation technique and the anti-beta-A4 immunostain.

Aged↗
PubMed1994

Unusual ubiquitin-positive glial cells in the globus pallidus of normal elderly human brains.

Unusual glial cells, inconspicuous in routine histological sections, were demonstrated in the globus pallidus using immunohistochemistry for anti-ubiquitin and a modified NOR-silver impregnation technique. These cells were identified as astrocytes and showed the following unusual features: (i) presence of intracytoplasmic vacuoles; (ii) immunoreactivity for ubiquitin; (iii) positive staining with a modified NOR-silver impregnation technique; and (iv) topographical location restricted to the globus pallidus. Quantitative analyses showed the numerical density of these cells to be significantly increased with normal ageing, whereas the presence of the cells was not related to pathological ageing or any other disease process. The data suggest that, not only in neurons but also in glial cells, accumulations of altered proteins can be found, which is probably due to a decline in the proteolytic activity of the cell.

Adult↗
PubMed1993

Synaptic stripping in the human facial nucleus.

An autopsy case of severe peripheral facial nerve paresis with disconnection of synapses from facial motor neurons is reported. A 77-year-old man presented with left-sided otitis media and subsequent development of facial nerve paresis. Three months later, the patient died of an acute gastrointestinal bleeding from a chronic duodenal ulcer. Gross inspection of the brain revealed non-stenosing arteriosclerotic vascular changes and a single small cystic lesion in the right putamen. Microscopically, marked chromatolytic changes were observed in the left facial nucleus. Immunocytochemistry for synaptophysin revealed a marked loss of afferent synaptic contacts from somatic and stem dendritic surface membranes of all chromatolytic motor neurons. Wrapping of a number of neurons by newly formed glial fibrillary acidic protein-positive astrocytic cell processes could be detected in the regenerating facial motor nucleus. In addition, expression of HLA-DR was increased on a small number of microglia and perivascular cells. These changes were absent from the contralateral, normal-appearing facial nucleus. To our knowledge, this case provides the first evidence for disconnection of synapses following peripheral nerve lesioning in humans. Occurrence of synaptic stripping is likely to explain nuclear hyperexcitability and failure of recovery of complex fine motor movements that are commonly observed following peripheral injury to the facial nerve.

Aged↗
PubMed1993

Pathological assessment of movement disorders: requirements for documentation in brain banks.

The general methodological requirements and principal morphologic hallmarks for the post mortem assessment of the major types of movement disorders are critically reviewed. These data may enable Brain Banks to classify movement disorders according to current clinicopathological diagnostic criteria. Comprehensive clinical assessment and accurate neuropathological examination using adequate methods are required for collection of and research on tissues from patients with movement disorders.

Brain Diseases↗
PubMed1992

Beta-endorphin: regional levels profile in the brain of the human infant.

Immunoradiometrical determinations of beta-endorphin (beta-EP) levels in 29 discrete brain regions from a series of victims of "Sudden Infant Death Syndrome" yielded a uniformly low levels profile in various areas of telencephalon, thalamus, pons, cerebellum and medulla oblongata. This low levels profile was interrupted by intermediate and high beta-EP levels in the midbrain and in two diencephalic zones. This study provides, for the first time, a comprehensive, neurochemically determined regional profile of beta-EP levels in the brain of the human infant.

Brain Chemistry↗
PubMed1991

Diffuse deposition of immunohistochemically labeled prion protein in the granular layer of the cerebellum in a patient with Creutzfeldt-Jakob disease.

Amyloid plaques in Creutzfeldt-Jakob disease, kuru, and Gerstmann-Sträussler-Scheinker syndrome are known to contain an abnormal isoform of a cellular protein, the prion protein (PrP). The prion protein in its normal cellular isoform is a membrane-bound glycoprotein of unknown function. The mechanisms causing a modification of PrP and accumulation in amyloid plaques are unknown. Here we present a case of Creutzfeldt-Jakob disease with widespread deposition of immunohistochemically labeled PrP in the internal granular layer of the cerebellum. Immunohistochemically labeled PrP was deposited in delicate granules, which often were associated with cellular processes or the cytoplams of undefined cells, or diffusely deposited in the neuropil.

Cerebellum↗