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Biomedical subjects

F Coria

Publications and source records attributed to F Coria.

At least 55 records · Page 3Linked to original sources
PubMed1993

[Efficacy of the proteic redistribution diet (PRD) in the antiparkinsonian effect of L-dopa].

The efficacy of PRD was evaluated in 21 patients with Parkinson's disease who presented motor fluctuations or a bad quality "on" time despite treatment with L-dopa or dopaminergic agonists. Eighteen of the 21 patients completed three months of treatment and only 14 (66.6%) were able to complete 12 months. The four patients who stopped treatment in this period did so because of subjective complaints despite obtaining good clinical response to PRD. Only three patients suspended the dietetic regime during first month of treatment. The 14 who completed the year of treatment showed a decrease in the "off" time (4.10 to 1.65: p < 0.01) and an improvement in motor response (14.89 to 10.39; p < 0.05) during the follow up period. Improvement appeared at the end of the second week of initiation of treatment. The diet was well tolerated with scarce complications, with only one patient presenting visual hallucinations. Other secondary effects were mild and did not require discontinuation of the diet. We conclude that proteic redistribution diet improves the "on" time in patients with Parkinson disease receiving L-dopa and delays the possibility of increasing the doses of L-dopa. The dietetic regimens with proteic redistribution seems a simple, useful and cheap approach without morbidity for the patients with Parkinson's disease showing a poor response or oscillation to L-dopa treatment.

Aged↗
PubMed1993

Acetylator polymorphism in Alzheimer's disease.

OBJECTIVES: To elucidate whether any relationship exists between genetic acetylator polymorphism and the risk of developing Alzheimer's disease. METHODS: Acetylator polymorphism has been determined, using sulphamethazine, in 54 patients with Alzheimer's disease or senile dementia of Alzheimer type and in 93 age-matched controls. RESULTS: Thirty-one patients (57.4%) and 54 controls (58%) were classified as slow acetylators (non-significant difference). No relation was found between acetylator polymorphism and age at onset of disease and scores of Minimental examination and Blessed, Tomlinson & Roth scale in the group of patients with Alzheimer's disease/senile dementia of Alzheimer type. CONCLUSIONS: Our results do not support the existence of any relationship between acetylator polymorphism and the risk of developing Alzheimer type dementia.

Acetylation↗
PubMed1992

Distribution of Alzheimer's disease amyloid protein precursor in normal human and rat nervous system.

Alzheimer's disease and cerebral amyloid angiopathies (CAA) are clinically heterogeneous diseases, but pathogenically related by the deposition of beta A4-amyloid in the brain in the form of neuritic plaques and/or vascular infiltrates. Antibodies directed against the N-terminal region of the predicted sequence of the beta A4 amyloid protein precursor (APP) were used to investigate the cellular distribution of this protein in the brain of normal humans and rats. We found a widespread presence of APP throughout the nervous tissue, including neurons, blood vessels, meningeal membranes, choroid plexus and ependymal cells. The highest APP immunoreactivity in both species was found in neuronal cell bodies and their processes, and around blood vessels. These findings may account for the clinical, pathological and aetiological differences found among the beta A4-amyloidosis.

Adult↗
PubMed1991

Reversible Schwann cell hypertrophy in lead neuropathy.

Schwann cell hypertrophy is an early change observed in lead-induced neuropathy in the rat. In order to quantify this cell hypertrophy, a morphometric analysis of Schwann cell cytoplasmic and nuclear areas and their relationship to the cross-sectional area of the associated myelinated fibre was performed. The study was carried out on sural and peroneal nerves from three groups of adult rats. Group I was intoxicated with 4% lead acetate in the drinking water for 6 weeks; group II animals were treated as in group I and then restored to standard laboratory conditions for 30 days; and group III were controls. The results showed that: (a) after 6 weeks of lead exposure, cytoplasmic and nuclear areas were significantly greater in intoxicated, compared with control rats; (b) after 30 days recovery, Schwann cell cytoplasmic and nuclear areas did not differ from control rats.

Animals↗
PubMed1990

Distribution of the protease inhibitor alpha 1-antichymotrypsin in cerebral and systemic amyloid.

We performed immunocytochemical staining to study the distribution of serum protease inhibitors in cerebral and systemic amyloid deposits. In beta-protein amyloid deposits in Alzheimer's disease, Down's syndrome, age-related cerebral amyloidosis, sporadic cerebral amyloid angiopathy and hereditary cerebral hemorrhage with amyloidosis of Dutch origin, antibody to alpha 1-antichymotrypsin (ACT) stains senile plaques and vascular deposits. Immature plaques or preamyloid deposits, identified by their positive staining for beta-protein and negative staining for Congo red, which represents the earliest recognizable stages of amyloid deposition, are also labeled. We did not detect ACT in other chemically different forms of cerebral and systemic amyloid. None of the other inhibitors in this study, i.e. antithrombin III and alpha 2-macroglobulin, was detected in the amyloid deposits. Neurons and glial cells throughout the central nervous system in normal and amyloid-containing brains also bind ACT antibody. The results emphasize the close association of ACT with one type of cerebral amyloid (beta-amyloid diseases) as well as the failure to detect such an association in other chemically different forms of cerebral and systemic amyloids.

Amyloid↗
PubMed1988

Beta-protein deposition: a pathogenetic link between Alzheimer's disease and cerebral amyloid angiopathies.

Cerebral amyloid angiopathy (CAA) refers to a group of hereditary (hereditary cerebral hemorrhage with amyloidosis, HCHWA and sporadic (SCAA) disorders characterized by amyloid fibril deposition restricted to the leptomeningeal and cortical vasculature leading to recurrent hemorrhagic and/or ischemic accidents. On clinical and biochemical grounds, two forms of HCHWA can be distinguished. The amyloid subunit of the HCHWA of Icelandic origin is related to Cystatin C, while amyloid from patients of Dutch origin (HCHWA-D) is related to the beta-protein (or A4), the main component of vascular and plaque core amyloid in Alzheimer's disease (AD) and Down's syndrome (DS) [corrected]. SCAA is an increasingly recognized cause of stroke in normotensive individual amounting to 5-10% of all cerebrovascular accidents. We now report the isolation and partial amino acid sequence of the amyloid subunit from a case of SCAA and a new case of HCHWA-D. The recognition that a heterogeneous group of diseases are linked by similar pathological and chemical features suggests that diversity of etiological factors may promote a common pathogenetic mechanism leading to amyloid-beta (A beta) deposition, and open new ways of research in AD and CAA as they are related to dementia and stroke.

Alzheimer Disease↗
PubMed1988

Recovery of the early cellular changes induced by lead in rat peripheral nerves after withdrawal of the toxin.

A morphological and quantitative investigation was carried out in the peripheral nerves of adult rats, which were first exposed to 4% lead acetate in the drinking water and then restored to standard laboratory conditions. After six weeks of continuous lead exposure, the only cells involved were Schwann cells (SC) and endothelial cells (EC). As compared to age-matched controls, the most conspicuous changes observed by light and electron microscopy in these cells included the presence of nuclear inclusion bodies (NIB), cytoplasmic hypertrophy, mitochondrial abnormalities, an increased number of myelin-derived SC intracytoplasmic structures, and vesiculation of myelin sheaths. By counting the number of nuclear profiles containing NIB in semithin sections stained with basic fuchsin and methylene blue, we found that SC from predominantly cutaneous (sural) nerves were less vulnerable to lead than SC from mixed (peroneal) and muscular (tibial) nerves. With respect to EC, however, no significant differences were found among these three nerves. After termination of lead exposure, we observed a gradual decrease of most of the above cellular changes, which finally disappeared at day 30 post-intoxication. However, the number of myelin-related SC cytoplasmic bodies still remained above normal levels at the time of the termination of the experiment (60 days post-intoxication). The nature of the changes induced by lead in peripheral nerve cells as well as the rapid and nearly complete recovery suggest that they reflect a compensatory response to overcome the adverse effects of the lead on cell metabolism.

Animals↗
PubMed1988

Isolation and characterization of amyloid P component from Alzheimer's disease and other types of cerebral amyloidosis.

The presence of amyloid P-component (AP) within cerebral amyloid deposits was investigated by means of biochemical and immunocytochemical methods. Immunoperoxidase on formalin-fixed, paraffin-embedded tissue sections from Alzheimer's Disease, Down's Syndrome, asymptomatic age-related cerebral amyloidosis, sporadic cerebral amyloid angiopathy, hereditary cerebral hemorrhage with amyloidosis-Icelandic type, and hereditary cerebral hemorrhage with amyloidosis-Dutch type revealed the presence of AP in the affected vessel walls in all cases, and in parenchymal deposits resembling neuritic plaques of Alzheimer's disease, sporadic cerebral amyloid angiopathy, and hereditary cerebral hemorrhage with amyloidosis-Dutch type. A short digestion of tissue sections with pepsin was required for immunodetection of AP in these latter structures. After extraction of leptomeningeal amyloid fibrils, AP was characterized by sodium dodecyl sulfate-polyacrylamide-gel electrophoresis, Western blot, gel chromatography, and partial amino acid sequencing. Our results indicate that: (a) AP from cerebral amyloidosis has similar biochemical properties and homologous amino terminal sequence to AP from systemic amyloidosis; (b) AP is associated to a variety of brain amyloid deposits regardless of their chemical nature. The presence of AP, a serum protein, within the brain parenchyma points to an impairment of the blood-brain barrier in these diseases.

Alzheimer Disease↗
PubMed1987

Cytochemical characteristics of the axon membrane at nodes of Ranvier in resting, tetrodotoxin-blocked, and electrically stimulated peripheral nerves of the rat.

To test whether intraaxonal ferric ion-ferrocyanide staining at nodes of Ranvier is influenced by functional state of the nodal membrane, the tibial nerves of Sprague-Dawley rats were subjected to one of the following experimental procedures prior to fixation and staining: General anesthesia to induce nerves at rest, tetrodotoxin blocking of nerve activity, and high-frequency (100 Hz) electrical stimulation. In all cases most but not all nodes were stained. No statistically significant differences were found either in the percentage of total stained nodes or in the percentage of stained nodes from large- and small-diameter fibers among the three conditions tested. An explanation is offered to account for the apparent discrepancy between these results and those from other studies involving related cytochemical markers of the nodal apparatus.

Anesthesia, General↗
PubMed1987

Brain amyloid in normal aging and cerebral amyloid angiopathy is antigenically related to Alzheimer's disease beta-protein.

Amyloid deposition is a prominent feature of a number of brain disorders, in which amyloid fibrils are found within blood vessel walls, the neuropil (neuritic plaques), neurons (neurofibrillary tangles). These include Alzheimer's disease (AD), AD changes associated with Down's syndrome, neurologically asymptomatic amyloidosis, Parkinson dementia of Guam, hereditary cerebral hemorrhage with amyloidosis of Icelandic origin (HCHWA-I), hereditary cerebral hemorrhage with amyloidosis of Dutch origin (HCHWA-D), and sporadic cerebral amyloid angiopathy (SCAA). Recently it was shown that the amyloid deposits in AD, Parkinson dementia of Guam, and HCHWA-D are formed by a similar 4-kd polypeptide called beta-protein. Because the nature of the amyloid deposits in other types of cerebral amyloidosis is not known, we have conducted immunocytochemical studies on brains from autopsy cases of AD, HCHWA-D, SCAA and neurologically asymptomatic elderly individuals. Brains from two subjects without neurologic involvement were used as controls. Sections from these specimens were incubated with rabbit polyclonal antibodies against 1) a synthetic peptide of 28 residues (anti-SP28), homologous to the NH2-terminal sequence of the beta-protein, 2) the main amyloid component of the HCHWA-I, a variant of cystatin C, and 3) purified fraction of neurofibrillary tangles. In all cases, anti-SP28 antibody specifically stained amyloid deposits in leptomeningeal and cortical vessels and neuritic plaques. These findings demonstrate that the amyloid deposits of SCAA and aged brains are composed of a protein antigenically similar to AD, HCHWA-D, and Parkinson dementia of Guam beta-protein, suggesting that all of these clinically and etiologically different morbid conditions are pathogenetically related. On this basis, they can be tentatively grouped as beta-protein deposition diseases. In addition, we found that HCHWA-D and SCAA vessels were mainly affected, while in AD parenchymal involvement predominates. These differences in the localization and extent of beta-protein deposits may account from the predominance of vascular complications in HCHWA-D and SCAA and of dementia in AD.

Aging↗
PubMed1986

Astrocyte culture on nitrocellulose membranes and plastic: detection of cytoskeletal proteins and mRNAs by immunocytochemistry and in situ hybridization.

Neonatal rat brain astrocyte secondary cultures were established on nitrocellulose membrane filters (13-mm diameter Millipore disk) and on plastic coverslips in serum-supplemented medium. On these substrata, cultured astrocytes changed their shape from flat and polygonal to stellate in the absence of hormones or growth factor supplements. Cultures became confluent after 4 days, and astrocytes on nitrocellulose filters continued to differentiate morphologically and biochemically, as evidenced by extensive cytoplasmic process formation and glial fibrillary acid protein (GFAP) accumulation. Cultures were immunostained for GFAP and vimentin. mRNAs to GFAP, vimentin, alpha and beta tubulin, and actin also were detected by in situ hybridization with biotinylated cDNA probes. The astrocyte culture method on nitrocellulose provides a simple, versatile means of comparing undifferentiated, morphologically mature, reactive, and neoplastic astrocytes in vitro.

Animals↗
PubMed1986

Hereditary motor and sensory neuropathy type II. Clinicopathological study of a family.

A family with hereditary motor and sensory neuropathy (HMSN) type II is described in which 10 affected and 17 unaffected members in three generations were examined. The peak age of onset was in the second decade. In the youngest generation, the proportion of affected to unaffected individuals at risk significantly differed from the expected 50%. There was slight slowing of conduction velocities in 36% of nerves; however, only 3 out of 10 affected members had entirely normal conduction studies. The amplitude of the sensory potentials of median and peroneal nerves was almost uniformly reduced. In all affected patients electromyography of anterior tibial muscles showed signs of neurogenic involvement. Histological study of two sural nerves and a sciatic nerve and its branches revealed loss of myelinated fibres with a proximal-to-distal gradient in this fibre loss, clusters of small regenerating fibres, and atrophic axons. Postmortem study of the proband showed loss of anterior horn and dorsal root ganglion neurons in the lumbar and sacral segments and degeneration of the fasciculus gracilis. Morphometric evaluation of L5 ventral and dorsal roots revealed a normal number of myelinated fibres, diameter histograms being shifted to the left because of a significant loss of large myelinated fibres and regeneration. These anatomical findings are consistent with the hypothesis that HMSN type II represents a primary neuronopathy affecting motor and sensory neurons.

Adult↗
PubMed1986

Laminated cytoplasmic bodies in Schwann cells and phagocytes: an ultrastructural and cytochemical study in the normal and lead-damaged peripheral nervous system of the rat.

We studied the distribution and cytochemical characteristics of laminated bodies (LBs) in the peripheral nervous system of normal and lead-intoxicated rats. In normal rats, LBs were exclusively present in myelin-forming Schwann cells (SCs). Nerves from lead-intoxicated animals showed extensive demyelination and remyelination. In these nerves we found an increase of LBs in the SC cytoplasm, and also within phagocytes involved in myelin removal, but not in remyelinating SCs. Cytochemical studies revealed that LBs were positive for acid phosphatase, thus demonstrating the lysosomal nature of such inclusions. Taken together, these data suggest that LBs are autophagolysosomes derived from myelin catabolism, which may be enhanced in the lead-induced demyelinating neuropathy of the rat. The possible mechanisms underlying this phenomenon and their pathological relevance are discussed.

Acid Phosphatase↗