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Rampello L.,University of Catania | Casolla B.,University of Rome La Sapienza | Pignatelli M.,University of Rome La Sapienza | Battaglia G.,Istituto Neurologico Mediterraneo Neuromed | And 3 more authors.
Multiple Sclerosis Journal | Year: 2011

The delayed conditioned eyeblink reflex, in which an individual learns to close the eyelid in response to a conditioned stimulus (e.g. a tone) relies entirely on the functional integrity of a cerebellar motor circuitry that involves the contingent activation of Purkinje cells by parallel and climbing fibres. Molecular changes that disrupt the function of this circuitry, in particular a loss of type-1 metabotropic glutamate receptors (mGlu1 receptors), occur in Purkinje cells of patients with multiple sclerosis and in mice with experimental autoimmune encephalomyelitis as a result of neuroinflammation. mGlu1 receptors are required for cerebellar motor learning associated with the conditioned eyeblink reflex. We propose that the delayed paradigm of the eyeblink conditioning might be particularly valuable for the detection of subtle abnormalities of cerebellar motor learning that are clinically silent and are not associated with demyelinating lesions or axonal damage. In addition, the test might have predictive value following a clinically isolated syndrome, and might be helpful for the evaluation of the efficacy of drug treatment in multiple sclerosis. © SAGE Publications 2011.

Loffredo L.,University of Rome La Sapienza | Perri L.,University of Rome La Sapienza | Di Castelnuovo A.,Laboratory of Molecular and Nutritional Epidemiology | Iacoviello L.,Laboratory of Molecular and Nutritional Epidemiology | And 2 more authors.
Nutrition, Metabolism and Cardiovascular Diseases | Year: 2015

Background and aims: Previous meta-analyses of interventional trials with vitamin E provided negative results but it remains unclear if this vitamin has some influence on cardiovascular events when supplemented alone. The aim of this study was to compare the effect of vitamin E alone or in combination with other antioxidants on myocardial infarction. Methods and results: Pubmed, ISI Web of Science, SCOPUS and Cochrane database were searched without language restrictions. We investigated randomized clinical trials studying the effect of vitamin E supplementation on myocardial infarction. Sixteen randomized controlled trials of vitamin E treatment were analyzed in this meta-analysis. The dose range for vitamin E was 33-800. IU. Follow-up ranged from 0.5 to 9.4 years. Compared to controls, vitamin E given alone significantly decreased myocardial infarction (3.0% vs 3.4%) (random effects R.R.: 0.82; 95% C.I., 0.70-0.96; p=0.01). This effect was driven by reduction of fatal myocardial infarction (random effects R.R.: 0.84; 95% C.I., 0.73-0.96; p=0.01). Conclusions: When supplemented alone, vitamin E reduces myocardial infarction in interventional trials while it appears ineffective when associated with other antioxidants. © 2015 Elsevier B.V.

Rampello L.,University of Catania | Malaguarnera M.,University of Catania | Nicoletti G.,Ospedale Garibaldi | Battaglia G.,Istituto Neurologico Mediterraneo Neuromed
Clinical Neurology and Neurosurgery | Year: 2012

Stabbing headache is a relatively rare type of chronic "primary" headache with distinctive features with respect to more common forms of paroxysmal headache, such as cluster headache and trigeminal neuralgia. Drug treatment is empirical because of the lack of knowledge on the pathophysiology of stabbing headache. We examined 26 patients recruited over 10 years, who met the diagnostic criteria for stabbing headache. Interestingly, more than half of these patients had autoimmune disorders, including multiple sclerosis, Sjögren's disease, Systemic Lupus Erythematosus, Behçet's disease, autoimmune vasculitis, and antiphospholipid antibody syndrome. We speculate that stabbing headache may develop as a result of neuroinflammation and, at least in some cases, may be an epiphenomenon of focal demyelinating lesions of the upper or lower brain stem. © 2011 Elsevier B.V. All rights reserved.

Spampinato S.F.,University of Catania | Merlo S.,University of Catania | Molinaro G.,Istituto Neurologico Mediterraneo Neuromed | Battaglia G.,Istituto Neurologico Mediterraneo Neuromed | And 3 more authors.
Endocrinology | Year: 2012

Pretreatment with 10 nM 17β-estradiol (17βE2) or 100 μM of the metabotropic glutamate 1 receptor (mGlu1R) agonist, dihydroxyphenylglycine (DHPG), protected neurons against N-methyl-D-aspartate (NMDA) toxicity. This effect was sensitive to blockade of both estrogen receptors and mGlu1R by their respective antagonists. In contrast, 17βE2 and/or DHPG, added after a low-concentration NMDA pulse (45 μM), produced an opposite effect, i.e. an exacerbation of NMDA toxicity. Again this effect was prevented by both receptor antagonists. In support of an interaction of estrogen receptors and mGlu1R in mediating a neurotoxic response, exacerbation of NMDA toxicity by 17βE2 disappeared when cultures were treated with DHPG prior to NMDA challenge, and conversely, potentiation of NMDA induced cell death by DHPG was prevented by pretreatment with 17βE2. Addition of calpain III inhibitor (10μM), 2 h before NMDA, prevented the increased damage induced by the two agonists, an affect that can be secondary to cleavage of mGlu1R by calpain. Accordingly, NMDA stimulation reduced expression of the full-length (140 kDa) mGluR1, an effect partially reversed by calpain inhibitor. Finally, in the presence of NMDA, the ability of 17βE2 to stimulate phosphorylation of AKT and ERK was impaired. Pretreatment with calpain inhibitor prevented the reduction of phosphorylated ERK but had no significant effect on phosphorylated AKT. Accordingly, the inhibition of ERK signaling by U0126 (1 μM) counteracted the effect of calpain inhibition on 17βE2-induced exacerbation of NMDA toxicity. The present data confirm the dual role of estrogens in neurotoxicity/neuroprotection and highlight the role of the timing of exposure to estrogens. Copyright © 2012 by The Endocrine Society.

Mirabella G.,Istituto Neurologico Mediterraneo Neuromed | Mirabella G.,University of Rome La Sapienza | Iaconelli S.,Istituto Neurologico Mediterraneo Neuromed | Modugno N.,Istituto Neurologico Mediterraneo Neuromed | And 3 more authors.
PLoS ONE | Year: 2013

A fundamental function of the motor system is to gather key information from the environment in order to implement behavioral strategies appropriate to the context. Although several lines of evidence indicate that Parkinson's disease affects the ability to modify behavior according to task requirements, it is currently unknown whether deep brain stimulation (DBS) of the subthalamic nucleus (STN) affects context-related planning. To explore this issue, we asked 12 Parkinson's patients with bilateral STN DBS and 13 healthy subjects to execute similar arm reaching movements in two different paradigms: go-only and countermanding tasks. In the former task patients had to perform speeded reaching movements to a peripheral target. In contrast, in the countermanding task participants had to perform the same reaches unless an infrequent and unpredictable stop-signal was shown during the reaction time (RT) indicating that they should withhold the ongoing action. We compared the performance of Parkinson's patients in different DBS conditions. We found that patients with both DBS-ON behaved similarly to healthy subjects, in that RTs of no-stop trial increased while movement times (MTs) decreased with respect to those of go-only-trials. However, when both DBS were off, both RTs and MTs were longer in no-stop trials than in go-only trials. These findings indicate that bilateral DBS of STN can partially restore the appropriate motor strategy according to the given cognitive contexts. © 2013 Mirabella et al.

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