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Biomedical subjects

S Sorbi

Publications and source records attributed to S Sorbi.

123 records · Page 7Linked to original sources
PubMed1982

Changes in high affinity choline uptake in rat cortex following lesions of the magnocellular forebrain nuclei.

High affinity choline uptake (HACU) and choline acetyltransferase (CAT) were measured in the cerebral cortex of rats 4 and 20 days after placing electrolytic lesions in the magnocellular forebrain nuclei (MFN) or in the pallidum. Four days after MFN lesion a 40-50% decrease in ipsilateral cortical HACU was found and a slightly smaller decrease was found 4 days after the pallidum lesion. Twenty days after the lesion, HACU activity returned to control values in the ipsilateral parietal cortex, its decrease was smaller than 4 days postlesion in the ipsilateral frontal cortex and a significant increase was found in the contralateral cortex. CAT activity showed a 40% decrease in the frontal, parietal and occipital ipsilateral cortex 4 days after MFN lesion. The same decrease was found 20 days postlesion. However, at this time a significant increase in CAT activity was detected in the contralateral cortex. The ipsilateral recovery of HACU activity 20 days after the lesions and the contralateral increase in HACU and CAT activity demonstrate the remarkable and widespread functional adjustment associated with discrete brain lesions. The existence of a large cholinergic pathway projecting to the neocortex from the basal forebrain region is also confirmed.

Animals↗
PubMed1982

Abnormal activation of pyruvate dehydrogenase in Leigh disease fibroblasts.

Incubation with dichloroacetate increased activity of the pyruvate dehydrogenase complex (PDHC) in disrupted fibroblasts from controls but not from two patients with autopsy-proved Leigh disease. These results are consistent with a genetically determined aberration of the regulation of PDHC in this disorder, although further studies are necessary to define the aberration.

Brain Diseases↗
PubMed1981

Spectrophotometric measurement of pyruvate dehydrogenase complex activity in cultured human fibroblasts.

A spectrophotometric assay for the pyruvate dehydrogenase complex (PDHC) has been adapted for use with cultured human fibroblasts. It is a coupled enzyme assay utilizing pigeon liver arylamine acetyltransferase to measure the acetyl-CoA produced by PDHC. Activity is proportional to fibroblast protein and to time and depends completely on added pyruvate, CoA and NAD. In extracts in which PDHC had been activated (dephosphorylated) by the method of Sheu et al. (Sheu, R.K.-F., Hu, C.C. and Utter, M.F. (1981) J. Clin. Invest. 67, 1463-1471), activities in control cell lines are 5-50-fold higher than in earlier reports. Low activity has been demonstrated in a line previously reported to be PDHC-deficient.

Acetyltransferases↗
PubMed1981

Choline acetyltransferase (ChAT) activity differs in right and left human temporal lobes.

Choline acetyltransferase (ChAT) activity was studied in different areas and in sequential sections of the cortical layers in the first temporal gyrus of left and right hemispheres of four human brains. The ChAT activity values obtained in all the samples from left hemisphere were significantly higher than in the right hemisphere. Furthermore, the study of ChAT activity in the cortical layers in Brodmann area 22 shows a greater left prevalence of enzymatic activity in cortical layers II and IV. The biochemical data seem to suggest a possible morphologic and/or functional difference between the two hemispheres.

Aged↗
PubMed1980

Biochemical differences between the left and right hemispheres. Preliminary observations on choline acetyl transferase (CAT) activity.

Choline acetyltransferase (CHAT) activity was studied in different areas in the first temporal gyrus of left and right hemispheres of human brains. The CHAT activity values obtained in all the samples from left hemisphere wee significantly higher than in the right hemisphere. The biochemical data seems to suggest a possible morphological and/or functional differences between the two hemispheres.

Aged↗
PubMed1980

Choline acetyltransferase and acetylcholinesterase abnormalities in senile dementia: importance of biochemical measurements in human post-mortem brain specimens.

Choline acetyltransferase and acetylcholinesterase have been assessed in human aging brains, in demented and agonal states. Choline acetyl transferase decreased during aging in normal brain when measured in the cerebral cortex. Choline acetyltransferase was also reduced in several other brain areas in patients with Alzheimer's disease and in one patient with Creutzfeldt-Jakob disease. Choline acetyltransferase was also reduced in bronchopneumonia and in some terminal conditions. On the contrary, the activity was not reduced in patients who died after cerebrovascular accidents. Acetylcholine esterase, although it followed the general trend of choline acetyltransferase, did not yield significant results.

Acetylcholinesterase↗
PubMed1980

Choline high-affinity uptake and metabolism and choline acetyltransferase activity in the striatum of rats chronically treated with neuroleptics.

High-affinity uptake of choline and choline acetyltransferase activity (ChAT) were measured in the striatum of rats treated for 45-60 days with haloperidol (1 mg/kg per os) and pimozide (1 mg/kg per os) daily and with fluspirilene (1 mg/kg i.m.) twice a week. Haloperidol and fluspirilene caused a 20%, and pimozide a 38%, increase in high-affinity uptake of choline. They also caused a significant decrease in ChAT activity: haloperidol, 20%; pimozide, 27%; and fluspirilene, 42%. In rats treated with fluspirilene for 65-80 days the metabolism of [3H] choline taken up by striatal synaptosomes was investigated. A 33% increase in total radioactivity, a significant increase in labelled acetylcholine (ACh), a relative decrease in labelled choline, and no change in labelled phosphorylcholine and betaine were found. It is concluded that the increase in high-affinity choline uptake caused by chronic administration of neuroleptic drugs is associated with a parallel increase in choline utilization for ACh formation. On the other hand, the decrease in ChAT activity does not appear to influence ACh formation.

Animals↗
PubMedDate not supplied

Free D-amino acids in human cerebrospinal fluid of Alzheimer disease, multiple sclerosis, and healthy control subjects.

This is the first report of the presence of free D-amino acids in lumbar and ventricular human cerebrospinal fluid (CSF) of individuals with Alzheimer disease (AD) compared with CSF of normal control subjects and with individuals affected by multiple sclerosis, as an unrelated neurologic disorder. Free D-amino acids are present at significantly higher levels in AD CSF than normal CSF, whereas in the CSF of patients affected by multiple sclerosis, D-amino acids occurs at the same level as in the normal controls. The total D-amino acid content in ventricular CSF was 1.48 times higher in the AD than controls (26.4 vs 17.9 nmol/mL, p = 0.025). The total D-amino acid content was 1.43 times higher in AD lumbar CSF than controls (1.89 vs 1.32 nmol/mL, p = 0.001). D-Aspartate in particular was 2.74 times higher in AD ventricular CSF compared to normal ventricular CSF (3.34 vs 1.22 nmol/mL, p = 0.029). In lumbar CSF, D-aspartate was 1.5 times higher in AD than controls (0.054 vs 0.036 nmol/mL, p = 0.041). Previously we reported that D-amino acids are elevated in AD brain proteins associated with neurofibrillary tangles compared to normal brain proteins (D'Aniello et al., 1992c; Fisher et al., 1992a,b). Thus, the D-amino acids present in CSF may originate from degradation of brain proteins.

Alzheimer Disease↗
PubMedDate not supplied

Growth properties of familial Alzheimer skin fibroblasts during in vitro aging.

Human diploid fibroblasts undergo replicative senescence in vitro, which is strongly correlated with biological aging in vivo. In order to examine whether features compatible with a systemic premature aging are present in familial Alzheimer's disease (FAD) patients, we investigated the growth characteristics of three skin fibroblast lines from FAD patients and from three sex/age-matched controls at different passages until senescence was reached. A kinetic study of the replicative capacity was performed at different culture times by [3H]-thymidine incorporation and crystal violet staining. Data showed no significant difference between the two groups at any studied passage. The life span of the two types of cultures was also comparable. These results suggest that in familial Alzheimer patients there are not systemic signs of accelerated aging.

Adult↗
PubMedDate not supplied

Clinical and genetic analysis of hereditary and sporadic ataxia in central Italy.

We have clinically and genetically evaluated 24 affected patients belonging to 22 Italian Friedreich ataxia (FA) families, 52 patients from 32 kindreds with proven autosomal dominant cerebellar ataxia (ADCA), 9 patients belonging to 5 families with autosomal recessive hereditary ataxia (ARCA) and 103 sporadic cases, 89 of which affected by idiopathic late onset cerebellar ataxia (ILOCA). Genotype-phenotype correlation analyses in FA patients have evidenced an inverse relationship between GAA repeat expansion length and age of onset, disease duration, and presence of cardiomyopathy. Among autosomal dominant types, spinocerebellar ataxia 2 (SCA2) genotype has been found in 31% of our ADCA families, resulting the most frequent form of ataxia. Phenotypic analysis of the various SCA subtypes evidenced a marked heterogeneity of symptoms with a substantial overlap between different syndromes.

Adult↗
PubMedDate not supplied

Double-blind, crossover, placebo-controlled clinical trial with L-acetylcarnitine in patients with degenerative cerebellar ataxia.

Despite the different genetic defects underlying degenerative ataxias, it has been suggested that mitochondrial energy production and antioxidative metabolism dysfunction may be common biochemical alterations related to these diseases. Acetylcarnitine, a cholinomimetic substance, is involved in oxidative metabolism and is a potential source of acetyl groups for the synthesis of acetylcholine in the mammalian brain. To determine whether treatment with L-acetylcarnitine may improve some clinical conditions of patients with ataxia, a double-blind crossover study with L-acetylcarnitine was performed in 24 patients with degenerative cerebellar diseases. Patients were selected from an ongoing prospective follow-up study at the Department of Neurology at the University of Florence, Italy. Each treatment phase with L-acetylcarnitine or placebo lasted 6 months, after which patients were crossed over to the other treatment phase. Ataxia was documented and quantified with use of a clinical score. After the trial, we observed a statistically significant improvement of some symptoms and a slow progression of the disease in both groups of patients.

Acetylcarnitine↗
PubMedDate not supplied

Are premorbid personality traits linked to the risk of Alzheimer's Disease? A case series of subjects with familial mutation.

BACKGROUND: The identification of the premorbid manifestation of Alzheimer's disease (AD) usually is carried out retrospectively by eliciting information from caregivers. However, the study of subjects with familial Alzheimer's disease (FAD) not yet affected by AD allows the direct identification of premorbid characteristics of the disease. METHODS: This is a psychometric assessment of 3 mutated and 5 control subjects, belonging to an Italian family associated with a missense mutation linked to the presenilin 2 gene. The assessment included an evaluation of personality traits, cognitive and affective condition, social disabilities, experiential and familial context. RESULTS: According to the MMPI, the mutated subjects did not show consistent personality traits. Also other questionnaires (HADS, WAIS, BDQ) were negative for definite cognitive or behavioural patterns. ApoE genotypes did not differentiate mutated from control subjects. CONCLUSIONS: Our results may be considered important for a better understanding of the pathogenesis of AD. The heuristic and practical importance of longitudinal prospective studies is emphasised.

Adult↗
PubMedDate not supplied

[Hexokinase in Alzheimer's disease].

Decreased hexokinase activity has been reported in brain, fibroblast, leukocytes and microvessels of patients with Alzheimer's disease. In this paper the results of an investigation on hexokinase activity in an Italian large pedigree are reported. The activity was comparable with that of the normal controls. These results suggest that Alzheimer's disease may be an heterogenic disorder.

Aged↗
PubMedDate not supplied

Is dementia primarily a subcortical disease? Appraisal of recent biochemical observations.

Recent studies have shown some morphological, structural, metabolic, and biochemical alterations in cortical and subcortical areas of brain of patients with Dementia. In this work we have studied Choline Acetyltransferase activity in cortical and subcortical areas and we present some data that shown a involvement of subcortical structures in Demented brain.

Aged↗