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335 results on '"Gualtieri, F."'

11. Neurogenesis impairment and increased cell death reduce total neuron number in the hippocampal region of fetuses with Down syndrome

Author

GUIDI, SANDRA, CECCARELLI, CLAUDIO, CIANI, ELISABETTA, BARTESAGHI, RENATA, Bonasoni P, Santini D, Gualtieri F, Guidi S, Bonasoni P, Ceccarelli C, Santini D, Gualtieri F, Ciani E, and Bartesaghi R

Subjects
NEUROGENESIS, DENTATE GYRUS, MENTAL RETARDATION, TRISOMY 21, HIPPOCAMPUS
Abstract

We previously obtained evidence for reduced cell proliferation in the dentate gyrus (DG) of fetuses with Down syndrome (DS), suggesting that the hippocampal hypoplasia seen in adulthood may be caused by defective early neuron production. The goal of this study was to establish whether DS fetuses (17-21 weeks of gestation) exhibit reduction in total cell number in the DG, hippocampus and parahippocampal gyrus (PHG). Volumes of the cellular layers and cell number were estimated with Cavalieri's principle and the optical fractionator method, respectively. We found that in DS fetuses all investigated structures had a reduced volume and cell number. Analysis of cell phenotype showed that DS fetuses had a higher percentage of cells with astrocytic phenotype but a smaller percentage of cells with neuronal phenotype. Immunohistochemistry for Ki-67, a marker of cycling cells, showed that DS fetuses had less proliferating cells in the germinal zones of the hippocampus and PHG. We additionally found that in the hippocampal region of DS fetuses there was a higher incidence of apoptotic cell death. Results show reduced neuron number in the DS hippocampal region and suggest that this defect is caused by disruption of neurogenesis and apoptosis, two fundamental processes underlying brain building.

Published
2008

13. Presynaptic Cholinergic Modulators as Potent Cognition Enhancers and Analgesic Drugs. 2. 2-Phenoxy-, 2-(Phenylthio)-, and 2-(Phenylamino)alkanoic Acid Esters

Author

Gualtieri, F., Bottalico, C., Calandrella, A., Dei, S., Giovannoni, M. P., Mealli, S., Romanelli, M. N., Scapecchi, S., Teodori, E., Nicoletta Galeotti, Ghelardini, C., Giotti, A., and Bartolini, A.

Subjects
Stereochemistry, Analgesic, Acetates, Nootropic, Mice, Structure-Activity Relationship, Cognition, Drug Discovery, Muscarinic acetylcholine receptor, medicine, Animals, Analgesics, Molecular Structure, Chemistry, Stereoisomerism, Biological activity, Acetylcholine, Mechanism of action, Synapses, Morphine, Molecular Medicine, Cholinergic, Analgesia, Propionates, medicine.symptom, Enantiomer, Tropanes, medicine.drug
Abstract

Further modifications of the leads ((R)-(+)-hyoscyamine and (p-chlorophenyl)propionic acid alpha-tropanyl ester), which show analgesic and nootropic activities as a consequence of increased central presynaptic ACh release, are reported. 2-Phenoxy- and 2-(phenylthio)alkanoic acid esters showed the best results. Several members of these classes possess analgesic properties which are comparable to that of morphine and at the same time are able to reverse dicyclomine-induced amnesia. Confirmation was found that the mechanism of action is due to an increase in ACh release at central muscarinic synapses and that both auto- and heteroreceptors controlling ACh release are very likely involved. According to the results obtained with (R)-(+)-hyoscyamine, analgesic activity is stereochemistry dependent, since the R-(+)-enantiomers are always more efficacious than the corresponding S-(-)-ones. On the basis of their potency and acute toxicity, compounds (+/-)-28 (SM21) and (+/-)-42 (SM32) were selected for further study.

Published
1994

14. Pathophysiogenesis of Mesial Temporal Lobe Epilepsy: Is Prevention of Damage Antiepileptogenic?

Author

Curia, G, Lucchi, C, Vinet, J, Gualtieri, F, Marinelli, C, Torsello, A, Costantino, L, Biagini, G, TORSELLO, ANTONIO BIAGIO, Biagini, G., Curia, G, Lucchi, C, Vinet, J, Gualtieri, F, Marinelli, C, Torsello, A, Costantino, L, Biagini, G, TORSELLO, ANTONIO BIAGIO, and Biagini, G.

Abstract

Temporal lobe epilepsy (TLE) is frequently associated with hippocampal sclerosis, possibly caused by a primary brain injury occurred a long time before the appearance of neurological symptoms. This type of epilepsy is characterized by refractoriness to drug treatment, so to require treatment with surgical resection of mesial temporal regions involved in seizure onset. Even this last therapeutic approach may fail in giving relief to patients. Although prevention of hippocampal damage and epileptogenesis after a primary event could be a key innovative approach to TLE, the lack of clear data on the pathophysiological mechanisms leading to TLE does not allow any rational therapy. Here we address the current knowledge on mechanisms supposed to be involved in epileptogenesis, as well as on the possible innovative treatments that may lead to a preventive approach. Besides loss of principal neurons and of specific interneurons, network rearrangement caused by axonal sprouting and neurogenesis are well known phenomena that are integrated by changes in receptor and channel functioning and modifications in other cellular components. In particular, a growing body of evidence from the study of animal models suggests that disruption of vascular and astrocytic components of the blood-brain barrier takes place in injured brain regions such as the hippocampus and piriform cortex. These events may be counteracted by drugs able to prevent damage to the vascular component, as in the case of the growth hormone secretagogue ghrelin and its analogues. A thoroughly investigation on these new pharmacological tools may lead to design effective preventive therapies.

Published
2014

18. Protective but not anticonvulsant effects of ghrelin and JMV-1843 in the pilocarpine model of Status epilepticus

Author

Lucchi, C, Curia, G, Vinet, J, Gualtieri, F, Bresciani, E, Locatelli, V, Torsello, A, Biagini, G, Biagini, G., BRESCIANI, ELENA, LOCATELLI, VITTORIO, TORSELLO, ANTONIO BIAGIO, Lucchi, C, Curia, G, Vinet, J, Gualtieri, F, Bresciani, E, Locatelli, V, Torsello, A, Biagini, G, Biagini, G., BRESCIANI, ELENA, LOCATELLI, VITTORIO, and TORSELLO, ANTONIO BIAGIO

Abstract

In models of status epilepticus ghrelin displays neuroprotective effects mediated by the growth hormone secretagogue-receptor 1a (GHS-R1a). This activity may be explained by anticonvulsant properties that, however, are controversial. We further investigated neuroprotection and the effects on seizures by comparing ghrelin with a more effective GHS-R1a agonist, JMV-1843. Rats were treated either with ghrelin, JMV-1843 or saline 10 min before pilocarpine, which was used to induce status epilepticus. Status epilepticus, developed in all rats, was attenuated by diazepam. No differences were observed among the various groups in the characteristics of pilocarpine-induced seizures. In saline group the area of lesion, characterized by lack of glial fibrillary acidic protein immunoreactivity, was of 0.45 ± 0.07 mm(2) in the hippocampal stratum lacunosum-moleculare, and was accompanied by upregulation of laminin immunostaining, and by increased endothelin-1 expression. Both ghrelin (P<0.05) and JMV-1843 (P<0.01) were able to reduce the area of loss in glial fibrillary acidic protein immunostaining. In addition, JMV-1843 counteracted (P<0.05) the changes in laminin and endothelin-1 expression, both increased in ghrelin-treated rats. JMV-1843 was able to ameliorate neuronal survival in the hilus of dentate gyrus and medial entorhinal cortex layer III (P<0.05 vs saline and ghrelin groups). These results demonstrate diverse protective effects of growth hormone secretagogues in rats exposed to status epilepticus.

Published
2013

30. Molecular Modulation of Muscarinic Antagonists. Synthesis and Pharmacological Profile of 2,2-diphenyl-2-ethylthioacetic and 3,3-diphenyl-3- ethylthiopropionic Acid Derivatives Characterized by a Dipeptide Spacer

Author

Scapecchi, S., primary, Martelli, C., additional, Angeli, P., additional, Bellucci, C., additional, Buccioni, M., additional, Dei, S., additional, Gualtieri, F., additional, Marucci, G., additional, Matucci, R., additional, and Romanelli, M., additional

Published
2004
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