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Biomedical subjects

E A Singh

Publications and source records attributed to E A Singh.

15 recordsLinked to original sources
PubMed1992

Apparent anterograde transport of basic fibroblast growth factor in the rat nigrostriatal dopamine system.

Five hours after the stereotaxic injection of approximately 1 ng of [125I]basic fibroblast growth factor (bFGF) into rat substantia nigra (SN), small but consistent amounts of radioactivity were found in the ipsilateral striatum (CP). None was found in the ipsilateral thalamus or contralateral CP, SN or thalamus. The amount found in the ipsilateral CP was very markedly reduced in rats injected 5-7 days after 6-hydroxydopamine-induced lesions of the nigrostriatal dopaminergic tract but was unaffected by prior kainic acid lesion of the CP. No radioactivity was found in the ipsilateral SN 5 h after injections of similar amounts of radioactive bFGF into the CP. These results are consistent with anterograde transport of bFGF in the dopaminergic nigrostriatal tract.

Animals↗
PubMed1992

Immunoblot detection of antibodies to myelin basic protein in Alzheimer's disease patients.

Based on a suspected pathological relationship of autoimmunity in Alzheimer's disease (AD), antibodies to myelin basic protein (MBP) were investigated in the sera of AD patients, healthy controls and disease controls. As detected by the protein-immunoblotting technique at a screening serum dilution of 1:400, sera from 16 of 18 (89%) AD patients were positive for antibodies to MBP. In contrast, sera from only 7 of 90 controls (healthy adults and elderlies, Parkinson's disease patients, mentally-retarded children and Down's syndrome patients) showed a positive reaction. This approximately 11-times higher incidence of antibodies to MBP in AD patients was statistically significant (P < or = 0.0001) and may indicate an autoimmune process in the pathophysiology of the disease.

Adult↗
PubMed1990

Binding of [3H]serotonin to lymphocytes in patients with neuropsychiatric disorders.

Based on recent studies of neuroimmune networks, the lymphocyte binding of serotonin neurotransmitter was studied in patients with Alzheimer's disease, idiopathic mental retardation, and autism. The specific binding to lymphocytes of [3H]serotonin, at a single concentration of 100 nM, was significantly reduced in Alzheimer's disease patients as compared to aged controls (group mean of 3.667 +/- 2.301 v 7.506 +/- 1.717 picomoles; p = 0.001), and in children with idiopathic mental retardation as compared to healthy children (group mean of 3.694 +/- 1.627 v 5.792 +/- 1.902 picomoles; p = 0.003). However, autistic children did not differ significantly from the healthy children (group mean of 5.287 +/- 1.987 v 5.792 +/- 1.902 picomoles; p = 0.475). Reduced lymphocyte binding of serotonin may be an indication of breakdown of an unknown neuroimmune pathway relevant to the pathophysiology of Alzheimer's disease and idiopathic mental retardation.

Aged↗
PubMed1988

Tetrahydroaminoacridine potentiates neurotoxicity of quinolinic acid in rat striatum.

Intraperitoneal injection of 5 mg/kg of tetrahydro-9-amino-acridine (THA) in rats 1 h before intrastriatal injection of 50-150 nmol of quinolinic acid potentiated the local neurotoxicity as indicated by measurements of striatal levels of glutamate decarboxylase and choline acetyltransferase. A larger dose (10 mg/kg) THA had no significant effect. The results are discussed in terms of THA's binding to various elements of the NMDA/sigma receptor complex and reported data on such binding are confirmed.

Aminoacridines↗
PubMed1988

Peripheral-type benzodiazepine binding in Alzheimer disease.

Peripheral-type benzodiazepine binding of [3H]Ro5-4864 at one, non-saturating concentration and activities of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) were measured in 7 cortical areas from postmortem brains of 18 patients with Alzheimer disease (AD), 12 age-matched controls, and 15 miscellaneous neurological cases. None of the chemical measures showed significant correlation with age, sex, or postmortem delay. As expected, ChAT and AChE activities were closely correlated with one another overall and within the AD and control groups, and the mean values for the AD group were significantly less than those in the controls in each of the cortical regions examined. Specific binding site densities were very variable from brain to brain and did not correlate with ChAT in any group or overall. By analysis of variance, however, binding site densities in the AD group were significantly higher than those in the controls. This difference was statistically significant (p less than 0.05) in Broca's area and the precentral and postcentral gyri, but not in the temporal gyri which generally have greater neuronal loss in AD. Of the 15 miscellaneous neurological cases, the Parkinson patients (n = 3) showed significantly higher binding densities than the controls but the multiinfarct dementia group (n = 5) did not. Single cases of Shy-Drager syndrome and sleep apnea showed a majority of values more than 2 standard deviations above the control means.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗
PubMed1987

gamma-Glutamyltransferase: normal cortical levels in Alzheimer disease.

gamma-Glutamyltransferase (EC 2.3.2.2; gamma-GT) may be important in the transport of amino acids or peptides across the blood-brain barrier. Gamma-GT activities were the same in cortical samples from Alzheimer and age-matched control brains, and there was no correlation between gamma-GT and choline acetyltransferase (ChAT) or acetylcholinesterase (AChE) levels, both of which were significantly reduced in the Alzheimer samples. ChAT and AChE activities were significantly correlated in both groups. ChAT showed a negative correlation with age in the controls and a positive correlation in the Alzheimer group. The opposite was true for gamma-GT, although the correlations were of low significance. The results do not lend any support to the hypothesis of a defect in the blood-brain barrier in Alzheimer disease.

Acetylcholinesterase↗
PubMed1979

Postnatal activity of angiotensin converting enzyme in rat brain.

The specific activity of angiotensin converting enzyme (ACE) was studied in eight brain regions in rats 2--65 days of age. At 65 days of age the activities in various regions relative to the cortex were: neostriatum, 1,200%; hippocampus/amygdala, 430%; hypothalamus, 190%; cerebellum, 140%; and midbrain, thalamus and pons/medulla, 110%. Significant linear increases were found in the neostriatum, hippocampus/amygdala and cortex at 2--65 days of age, in the pons/medulla and thalamus at 2--42 days of age and in the midbrain at 2--21 days of age. The increase with age was greatest in the neostriatum and the data are consistent with the occurrence of ACE in neurons in this area.

Aging↗
PubMedDate not supplied

Sodium-dependent glutamate binding in senile dementia.

Sodium-dependent glutamate binding was studied as a possible index of the integrity of glutamate/aspartate (Glu/Asp) nerve endings in seven cortical areas from postmortem brains of 15 persons with senile dementia of the Alzheimer type (SD), 10 controls matched for age, sex and postmortem delay (PMD), and single cases of Down's syndrome and Parkinson-dementia. Binding affinities (Kd) were quite variable from brain to brain but showed no relation to sex, age, PMD or disease. Specific binding site densities did not vary with age or sex but showed overall a significant negative correlation with PMD, a significant decrease in SD, and a significant correlation in the SD--but not the control--samples with choline acetyltransferase (ChAT) activities. The binding data on individual brain regions, however, showed no significant difference between SD cases and controls despite highly significant differences in the ChAT activities. The overall results support but do not confirm a defect in cortical Glu/Asp systems in SD. Reported and obtained data on lesioned rats are summarized to suggest that sodium-dependent glutamate binding may be an ineffective index of Glu/Asp nerve endings.

Acetylcholinesterase↗