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Caccavale, S., Bove, D., Bove, R.M., La Montagna, M.
Skin and brain: Itch and psychiatric disorders
(2016) Giornale Italiano di Dermatologia e Venereologia, 151 (5), pp. 525-529. 
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84988908294&partnerID=40&md5=276651a8dec70d97edb467009baa5ec8

AFFILIATIONS: Department of Mental and Physical Health and Preventive Medicine, Second University of Naples, Naples, Italy; 
Fusis Association for Research in Child and Adolescent Neuropsychiatry, Alvignano, Italy; 
Department of Clinical and Experimental Sciences, Section of Psychiatry and Clinical Psychology, University of Foggia, Via Antonio Gramsci, Foggia, Italy
ABSTRACT: Skin diseases (atopic eczema, psoriasis, idiopathic urticaria), systemic diseases (chronic hepatic or renal failure, morbus Hodgkin, diabetes mellitus) and psychiatric disorders (obsessive compulsive disorders, depression, delusions of parasitosis) can occur with itching. The aim of this review is to clarify the link between pruritus and psychiatric morbidity and emphasize the importance of a psychiatric consultation for patients with a chronic itching, without a skin disease. In the last years, there is a growing awareness regarding psychogenic itch, although these types of itch are significantly less studied in comparison to other types of pruritus. Psychogenic pruritus is usually a diagnosis of exclusion. There are not controlled studies about treatment of psychogenic itch, but the same drugs prescribed for neuropathic pain, depression, and anxiety are used. There is a strong association between pruritus and psyche; so, it is important that the dermatologist evaluates psychosomatic dimension. According to the analysis of scientific literature and our clinical experience, pruritus seems to be a rather common phenomenon in patients suffering from depression. Future works should explain the basis of psychopathology of chronic itching thanks to studies of selected groups of patients with a particular type of chronic itching, highlighting the clinical features to establish appropriate and individual targeted care, based on the several types of pruritus. Some questions still unanswered could be clarified in this way. It is really important to decrease the symptoms "itching", because the quality of life of the patient will be improved, but the goal is to identify the underlying mechanisms of itch and establish a targeted therapy, depending on the biological changes and the underlying disease. Copyright © 2016 Edizioni Minerva Medica.
AUTHOR KEYWORDS: Brain;  Mental disorders;  Pruritus;  Skin
CORRESPONDENCE ADDRESS: La Montagna, M.; Department of Clinical and Experimental Sciences, Section of Psychiatry and Clinical Psychology, University of Foggia, Via Antonio Gramsci, Italy; email: maddafly87@libero.it
DOCUMENT TYPE: Review

Scopus news

Caccavale, S., Bove, D., Bove, R.M., La Montagna, M.
Skin and brain: Itch and psychiatric disorders
(2016) Giornale Italiano di Dermatologia e Venereologia, 151 (5), pp. 525-529. 
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84988908294&partnerID=40&md5=276651a8dec70d97edb467009baa5ec8

AFFILIATIONS: Department of Mental and Physical Health and Preventive Medicine, Second University of Naples, Naples, Italy; 
Fusis Association for Research in Child and Adolescent Neuropsychiatry, Alvignano, Italy; 
Department of Clinical and Experimental Sciences, Section of Psychiatry and Clinical Psychology, University of Foggia, Via Antonio Gramsci, Foggia, Italy
ABSTRACT: Skin diseases (atopic eczema, psoriasis, idiopathic urticaria), systemic diseases (chronic hepatic or renal failure, morbus Hodgkin, diabetes mellitus) and psychiatric disorders (obsessive compulsive disorders, depression, delusions of parasitosis) can occur with itching. The aim of this review is to clarify the link between pruritus and psychiatric morbidity and emphasize the importance of a psychiatric consultation for patients with a chronic itching, without a skin disease. In the last years, there is a growing awareness regarding psychogenic itch, although these types of itch are significantly less studied in comparison to other types of pruritus. Psychogenic pruritus is usually a diagnosis of exclusion. There are not controlled studies about treatment of psychogenic itch, but the same drugs prescribed for neuropathic pain, depression, and anxiety are used. There is a strong association between pruritus and psyche; so, it is important that the dermatologist evaluates psychosomatic dimension. According to the analysis of scientific literature and our clinical experience, pruritus seems to be a rather common phenomenon in patients suffering from depression. Future works should explain the basis of psychopathology of chronic itching thanks to studies of selected groups of patients with a particular type of chronic itching, highlighting the clinical features to establish appropriate and individual targeted care, based on the several types of pruritus. Some questions still unanswered could be clarified in this way. It is really important to decrease the symptoms "itching", because the quality of life of the patient will be improved, but the goal is to identify the underlying mechanisms of itch and establish a targeted therapy, depending on the biological changes and the underlying disease. Copyright © 2016 Edizioni Minerva Medica.
AUTHOR KEYWORDS: Brain;  Mental disorders;  Pruritus;  Skin
CORRESPONDENCE ADDRESS: La Montagna, M.; Department of Clinical and Experimental Sciences, Section of Psychiatry and Clinical Psychology, University of Foggia, Via Antonio Gramsci, Italy; email: maddafly87@libero.it
DOCUMENT TYPE: Review

Scopus news

Mucci, A., Dima, D., Soricelli, A., Volpe, U., Bucci, P., Frangou, S., Prinster, A., Salvatore, M., Galderisi, S., Maj, M.
Is avolition in schizophrenia associated with a deficit of dorsal caudate activity? A functional magnetic resonance imaging study during reward anticipation and feedback
(2015) Psychological Medicine, 45 (8), pp. 1765-1778. 
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84988258835&partnerID=40&md5=1a4020fef7315d53ea234e5c89a8d025
DOI: 10.1017/S0033291714002943
AFFILIATIONS: Department of Psychiatry, University of Naples SUN, Largo Madonna delle Grazie, Naples, Italy; 
Psychosis Research Program, Department of Psychiatry, Icahn School of Medicine, Mount Sinai, NY, United States; 
MRC Social Genetic and Developmental Psychiatry, Institute of Psychiatry, King's College London, United Kingdom; 
University of Naples 'Parthenope', IRCCS Research Institute SDN, Naples, Italy; 
Biostructure and Bioimaging Institute, National Research Council, Naples, Italy; 
Department of Biomorphological and Functional Studies, University of Naples 'Federico II', Naples, Italy
ABSTRACT: Background The neurobiological underpinnings of avolition in schizophrenia remain unclear. Most brain imaging research has focused on reward prediction deficit and on ventral striatum dysfunction, but findings are not consistent. In the light of accumulating evidence that both ventral striatum and dorsal caudate play a key role in motivation, we investigated ventral striatum and dorsal caudate activation during processing of reward or loss in patients with schizophrenia. Method We used functional magnetic resonance imaging to study brain activation during a Monetary Incentive Delay task in patients with schizophrenia, treated with second-generation antipsychotics only, and in healthy controls (HC). We also assessed the relationships of ventral striatum and dorsal caudate activation with measures of hedonic experience and motivation. Results The whole patient group had lower motivation but comparable hedonic experience and striatal activation than HC. Patients with high avolition scores showed lower dorsal caudate activation than both HC and patients with low avolition scores. A lower dorsal caudate activation was also observed in patients with deficit schizophrenia compared to HC and patients with non-deficit schizophrenia. Dorsal caudate activity during reward anticipation was significantly associated with avolition, but not with anhedonia in the patient group. Conclusions These findings suggest that avolition in schizophrenia is linked to dorsal caudate hypoactivation. © Cambridge University Press 2015.
AUTHOR KEYWORDS: Avolition;  deficit schizophrenia;  dorsal caudate;  reward anticipation;  schizophrenia;  ventral striatum
CORRESPONDENCE ADDRESS: Mucci, A.; Department of Psychiatry, University of Naples SUN, Largo Madonna delle Grazie, Italy; email: armida.mucci@gmail.com
DOCUMENT TYPE: Article

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Babiloni, C., Del Percio, C., Caroli, A., Salvatore, E., Nicolai, E., Marzano, N., Lizio, R., Cavedo, E., Landau, S., Chen, K., Jagust, W., Reiman, E., Tedeschi, G., Montella, P., De Stefano, M., Gesualdo, L., Frisoni, G.B., Soricelli, A.
Cortical sources of resting state EEG rhythms are related to brain hypometabolism in subjects with Alzheimer's disease: an EEG-PET study
(2016) Neurobiology of Aging, 48, pp. 122-134. 
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DOI: 10.1016/j.neurobiolaging.2016.08.021
AFFILIATIONS: Department of Human Physiology and Pharmacology “Erspamer”, University of Rome “ La Sapienza”, Rome, Italy; 
Institute for Research and Medical Care, IRCCS San Raffaele Pisana, Rome, Italy; 
Department of Integrated Imaging, IRCCS SDN, Napoli, Italy; 
Medical Imaging Unit, IRCCS Istituto di Ricerche Farmacologiche Mario Negri, Bergamo, Italy; 
Department of Neurosciences, Reproductive Sciences and Odontostomatology, University of Naples Federico II, Naples, Italy; 
LENITEM Laboratory of Epidemiology, Neuroimaging, and Telemedicine, IRCCS Istituto Centro San Giovanni di Dio-Fatebenefratelli, Brescia, Italy; 
Cognition, Neuroimaging and Brain Diseases Laboratory, Centre de Recherche de l'Institut du Cerveau et de la Moelle Épiniére (CRICM-UMRS 975), Université Pierre et Marie Curie-Paris 6, Paris, France; 
Helen Wills Neuroscience Institute, University of California, Berkeley, CA, United States; 
Banner Alzheimer's Institute, Phoenix, AZ, United States; 
Department of Neurological Sciences, Second University of Naples, Naples, Italy; 
Dipartimento Emergenza e Trapianti d'Organi (D.E.T.O), University of Bari, Bari, Italy; 
Memory Clinic and LANVIE - Laboratory of Neuroimaging of Aging, University Hospitals and University of Geneva, Geneva, Switzerland; 
Department of Motor Sciences and Healthiness, University of Naples Parthenope, Naples, Italy
ABSTRACT: Cortical sources of resting state electroencephalographic (EEG) delta (2–4 Hz) and low-frequency alpha (8–10.5 Hz) rhythms show abnormal activity (i.e., current density) in patients with dementia due to Alzheimer's disease (AD). Here, we hypothesized that abnormality of this activity is related to relevant disease processes as revealed by cortical hypometabolism typically observed in AD patients by fluorodeoxyglucose positron emission tomography. Resting state eyes-closed EEG data were recorded in 19 AD patients with dementia and 40 healthy elderly (Nold) subjects. EEG frequency bands of interest were delta and low-frequency alpha. EEG sources were estimated in these bands by low-resolution brain electromagnetic tomography (LORETA). Fluorodeoxyglucose positron emission tomography images were recorded only in the AD patients, and cortical hypometabolism was indexed by the so-called Alzheimer's discrimination analysis tool (PALZ) in the frontal association, ventromedial frontal, temporoparietal association, posterior cingulate, and precuneus areas. Results showed that compared with the Nold group, the AD group pointed to higher activity of delta sources and lower activity of low-frequency alpha sources in a cortical region of interest formed by all cortical areas of the PALZ score. In the AD patients, there was a positive correlation between the PALZ score and the activity of delta sources in the cortical region of interest (p < 0.05). These results suggest a relationship between resting state cortical hypometabolism and synchronization of cortical neurons at delta rhythms in AD patients with dementia. © 2016 Elsevier Inc.
AUTHOR KEYWORDS: Alzheimer's disease (AD);  Brain hypometabolism;  Electroencephalography (EEG);  Fluorodeoxyglucose positron emission tomography (FDG-PET);  Low resolution brain electromagnetic tomography (LORETA)
CORRESPONDENCE ADDRESS: Lizio, R.; Department of Physiology and Pharmacology “V. Erspamer”, University of Rome “La Sapienza”, P.le A. Moro 5, Italy; email: roberta.lizio@uniroma1.it
DOCUMENT TYPE: Article

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Citraro, R., Russo, E., Leo, A., Russo, R., Avagliano, C., Navarra, M., Calignano, A., De Sarro, G.
Pharmacokinetic-pharmacodynamic influence of N-palmitoylethanolamine, arachidonyl-2′-chloroethylamide and WIN 55,212-2 on the anticonvulsant activity of antiepileptic drugs against audiogenic seizures in DBA/2 mice
(2016) European Journal of Pharmacology, 791, pp. 523-534. 
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DOI: 10.1016/j.ejphar.2016.09.029
AFFILIATIONS: Science of Health Department, Clinical Pharmacology Unit, School of Medicine, University “Magna Graecia” of Catanzaro, Italy; 
Department of Pharmacy, University of Naples “Federico II”Naples, Italy; 
Department of Experimental Pharmacology, University of MessinaMessina, Italy
ABSTRACT: We evaluated the effects of ACEA (selective cannabinoid (CB)1 receptor agonist), WIN 55,212-2 mesylate (WIN; non-selective CB1 and CB2 receptor agonist) and N-palmitoylethanolamine (PEA; an endogenous fatty acid of ethanolamide) in DBA/2 mice, a genetic model of reflex audiogenic epilepsy. PEA, ACEA or WIN intraperitoneal (i.p.) administration decreased the severity of tonic-clonic seizures. We also studied the effects of PEA, WIN or ACEA after co-administration with NIDA-41020 (CB1 receptor antagonist) or GW6471 (PPAR-α antagonist) and compared the effects of WIN, ACEA and PEA in order to clarify their mechanisms of action. PEA has anticonvulsant features in DBA/2 mice mainly through PPAR-α and likely indirectly on CB1 receptors, whereas ACEA and WIN act through CB1 receptors. The co-administration of ineffective doses of ACEA, PEA and WIN with some antiepileptic drugs (AEDs) was examined in order to identify potential pharmacological interactions in DBA/2 mice. We found that PEA, ACEA and WIN co-administration potentiated the efficacy of carbamazepine, diazepam, felbamate, gabapentin, phenobarbital, topiramate and valproate and PEA only also that of oxcarbazepine and lamotrigine whereas, their co-administration with levetiracetam and phenytoin did not have effects. PEA, ACEA or WIN administration did not significantly influence the total plasma and brain levels of AEDs; therefore, it can be concluded that the observed potentiation was only of pharmacodynamic nature. In conclusion, PEA, ACEA and WIN show anticonvulsant effects in DBA/2 mice and potentiate the effects several AEDs suggesting a possible therapeutic relevance of these drugs and their mechanisms of action. © 2016
AUTHOR KEYWORDS: Antiepileptic drugs;  Audiogenic seizure model;  Cannabinoid compounds;  Drug interaction;  PEA;  PPAR-α receptors
CORRESPONDENCE ADDRESS: De Sarro, G.; Science of Health Department, Clinical Pharmacology Unit, School of Medicine, University “Magna Graecia” of CatanzaroItaly; email: desarro@unicz.it
DOCUMENT TYPE: Article

Scopus news

Coccurello, R., Bisogno, T.
The bright side of psychoactive substances: cannabinoid-based drugs in motor diseases
(2016) Expert Review of Clinical Pharmacology, 9 (10), pp. 1351-1362. 
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DOI: 10.1080/17512433.2016.1209111
AFFILIATIONS: Institute of Cell Biology and Neurobiology (IBCN), National Research Council (C.N.R.), Roma, Italy; 
Fondazione S. Lucia (FSL- IRCCS), Neurochemistry of Lipids Lab, Roma, Italy; 
Endocannabinoid Research Group, Institute of Biomolecular Chemistry, National Research Council (C.N.R.), Pozzuoli, Italy; 
Department of Medicine, Campus Bio-Medico University of Rome, Roma, Italy
ABSTRACT: Introduction: Psychoactive substances are associated with the idea of drugs with high addictive liability, affecting mental states, cognition, emotion and motor behavior. However these substances can modify synaptic transmission and help to disclose some mechanisms underlying alterations in brain processing and pathophysiology of motor disease. Hence, the ‘bright side’ of e cannabinoid-based drugs must be thoroughly examined to be identified within the latter framework. Areas covered: We will analyze the preclinical and clinical evidence of cannabinoid-based drugs, discussing their therapeutic value in basal ganglia motor disorders such as Parkinson’s disease and Huntington disease. Expert commentary: Despite the knowledge acquired in the last years, the therapeutic potential of cannabinoid-based drugs should be further tested by novel routes of investigation. This should be focused on the role of cannabinoid signaling system in mitochondrial function as well as on the physical and functional interaction with other key receptorial targets belonging to this network. © 2016 Informa UK Limited, trading as Taylor & Francis Group.
AUTHOR KEYWORDS: cannabinoid-based drugs;  endocannabinoid system;  Huntington disease;  motor diseases;  neuroprotection;  Parkinson’s disease
CORRESPONDENCE ADDRESS: Coccurello, R.; Institute of Cell Biology and Neurobiology (IBCN), National Research Council (C.N.R.), IRCCS Fondazione S. Lucia (FSL), Via del Fosso di Fiorano 64, Italy; email: roberto.coccurello@cnr.it
DOCUMENT TYPE: Review

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Pezzini, A., Grassi, M., Lodigiani, C., Patella, R., Gandolfo, C., Zini, A., Delodovici, M.L., Paciaroni, M., Del Sette, M., Toriello, A., Musolino, R., Calabrò, R.S., Bovi, P., Adami, A., Silvestrelli, G., Sessa, M., Cavallini, A., Marcheselli, S., Marco Bonifati, D., Checcarelli, N., Tancredi, L., Chiti, A., Del Zotto, E., Tomelleri, G., Spalloni, A., Giorli, E., Costa, P., Giacalone, G., Ferrazzi, P., Poli, L., Morotti, A., Piras, V., Rasura, M., Simone, A.M., Gamba, M., Cerrato, P., Zedde, M.L., Micieli, G., Melis, M., Massucco, D., Guido, D., De Giuli, V., Bonaiti, S., D'Amore, C., La Starza, S., Iacoviello, L., Padovani, A.
Propensity Score-Based Analysis of Percutaneous Closure Versus Medical Therapy in Patients with Cryptogenic Stroke and Patent Foramen Ovale: The IPSYS Registry (Italian Project on Stroke in Young Adults)
(2016) Circulation: Cardiovascular Interventions, 9 (9), art. no. e003470, . 
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DOI: 10.1161/CIRCINTERVENTIONS.115.003470
AFFILIATIONS: Dipartimento di Scienze Cliniche e Sperimentali, Clinica Neurologica, Università degli Studi di Brescia, P.le Spedali Civili, 1, Brescia, Italy; 
Dipartimento di Scienze Del Sistema Nervoso e Del Comportamento, Unità di Statistica Medica e Genomica, Università di Pavia, Italy; 
Centro Trombosi, IRCCS Istituto Clinico Humanitas, Rozzano-Milano, Italy; 
Stroke Unit, Azienda Ospedaliera sant'Andrea, Università la Sapienza, Rome, Italy; 
Dipartimento di Neuroscienze, Riabilitazione, Oftalmologia, Genetica e Scienze Materno-Infantili, Università di Genova, Italy; 
Stroke Unit, Clinica Neurologica, Nuovo Ospedale Civile s. Agostino Estense, Modena, Italy; 
Unità di Neurologia, Ospedale di Circolo, Università dell'Insubria, Varese, Italy; 
Stroke Unit, Divisione di Medicina Cardiovascolare, Università di Perugia, Perugia, Italy; 
Unità di Neurologia, Ospedale Galliera, Genova, Italy; 
A.O Universitaria san Giovanni di Dio e Ruggi d'Aragona, Salerno, Italy; 
Dipartimento di Neuroscienze, Scienze Psichiatriche e Anestesiologiche, Clinica Neurologica, Università di Messina, Italy; 
IRCCS, Centro Neurolesi Bonino-Pulejo, Messina, Italy; 
UO Neurologia, Azienda Ospedaliera-Universitaria Borgo Trento, Verona, Italy; 
Stroke Center, Dipartimento di Neurologia, Ospedale Sacro Cuore Negrar, Verona, Italy; 
Stroke Unit, Dipartimento di Neuroscienze, Azienda Ospedaliera Carlo Poma, Mantova, Italy; 
U.O Neurologia, Istituti Ospitalieri, Cremona, Italy; 
Stroke Unit, IRCCS Fondazione Istituto c. Mondino Pavia, Italy; 
Neurologia d'Urgenza e Stroke Unit, IRCCS Istituto Clinico Humanitas, Rozzano-Milano, Italy; 
Stroke Unit, U.O Neurologia, Ospedale s. Chiara, Trento, Italy; 
U.O.C Neurologia, Ospedale Valduce, Como, Italy; 
U.O Neurologia, Azienda Ospedaliera Ospedale sant'Anna, Como, Italy; 
Neurologia, Azienda Ospedaliero Universitaria Pisana, Pisa, Italy; 
U.O Recupero e Rieducazione Funzionale, IRCCS Fondazione Don Gnocchi, Milan, Italy; 
Unità di Neurologia, Ospedale S. Andrea, La Spezia, Italy; 
Clinica Neurologia, IRCCS san Raffaele Milano, Italy; 
Stroke Unit, Azienda Ospedaliera g. Brotzu Cagliari, Italy; 
Stroke Unit, Neurologia Vascolare, Spedali Civili di Brescia, Italy; 
Dipartimento di Neuroscienze, Stroke Unit, Università di Torino, Italy; 
S.C. Neurologia, IRCCS Arcispedale santa Maria Nuova Reggio Emilia, Italy; 
Laboratorio di Epidemiologia Molecolare e Nutrizionale, Dipartimento di Epidemiologia e Prevenzione, IRCCS Istituto Neurologico Mediterraneo, Pozzilli, Italy
ABSTRACT: Background-We sought to compare the benefit of percutaneous closure to that of medical therapy alone for the secondary prevention of embolism in patients with patent foramen ovale (PFO) and otherwise unexplained ischemic stroke, in a propensity scored study. Methods and Results-Between 2000 and 2012, we selected consecutive first-ever ischemic stroke patients aged 18 to 45 years with PFO and no other cause of brain ischemia, as part of the IPSYS registry (Italian Project on Stroke in Young Adults), who underwent either percutaneous PFO closure or medical therapy for comparative analysis. Primary end point was a composite of ischemic stroke, transient ischemic attack, or peripheral embolism. Secondary end point was brain ischemia. Five hundred and twenty-one patients qualified for the analysis. The primary end point occurred in 15 patients treated with percutaneous PFO closure (7.3%) versus 33 patients medically treated (10.5%; hazard ratio, 0.72; 95% confidence interval, 0.39-1.32; P=0.285). The rates of the secondary end point brain ischemia were also similar in the 2 treatment groups (6.3% in the PFO closure group versus 10.2% in the medically treated group; hazard ratio, 0.64; 95% confidence interval, 0.33-1.21; P=0.168). Closure provided a benefit in patients aged 18 to 36 years (hazard ratio, 0.19; 95% confidence interval, 0.04-0.81; P=0.026) and in those with a substantial right-to-left shunt size (hazard ratio, 0.19; 95% confidence interval, 0.05-0.68; P=0.011). Conclusions-PFO closure seems as effective as medical therapy for secondary prevention of cryptogenic ischemic stroke. Whether device treatment might be more effective in selected cases, such as in patients younger than 37 years and in those with a substantial right-to-left shunt size, deserves further investigation. © 2016 American Heart Association, Inc.
AUTHOR KEYWORDS: atrial septum;  follow-up studies;  patent foramen ovale;  secondary prevention;  stroke
CORRESPONDENCE ADDRESS: Pezzini, A.; Dipartimento di Scienze Cliniche e Sperimentali, Clinica Neurologica, Università degli Studi di Brescia, P.le Spedali Civili, 1, Italy; email: ale_pezzini@hotmail.com
DOCUMENT TYPE: Article

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Conforti, R., Capasso, R., Galasso, R., Cirillo, M., Taglialatela, G., Galasso, L.
A challenging diagnosis of late-onset tumefactive multiple sclerosis associated to cervicodorsal syringomyelia: Doubtful CT, MRI, and bioptic findings Case report and literature review
(2016) Medicine (United States), 95 (36), art. no. e4585, . 
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DOI: 10.1097/MD.0000000000004585
AFFILIATIONS: Neuroradiology Service, Department of Radiology, Second University of Naples, Naples, Italy; 
Department of Internal Clinical and Experimental Medicine and Surgery, F. Magrassi-A. Lanzara Second University of Naples, Piazza Miraglia, Naples, Italy; 
Neuroradiology Department, San Luca Hospital, Vallo della Lucania, Salerno, Italy
ABSTRACT: Background: Tumefactive multiple sclerosis (MS) is an unusual variant of demyelinating disease characterized by lesions with pseudotumoral appearance on radiological imaging mimicking other space-occupying lesions, such as neoplasms, infections, and infarction. Especially when the patient's medical history is incompatible with MS, the differential diagnosis between these lesions constitutes a diagnostic challenge often requiring histological investigation. An older age at onset makes distinguishing tumefactive demyelinating lesion (TDL) from tumors even more challenging. Methods:We report a case of brain TDL as the initial manifestation of late-onset MS associated with cervico-dorsal syringomyelia. A 66-year-old Caucasian woman with a 15-day history headache was referred to our hospital because of the acute onset of paraphasia. She suffered from noncommunicating syringomyelia associated to basilar impression and she reported a 10-year history of burning dysesthesia of the left side of the chest extended to the internipple line level. Results: Computed tomography (CT) and magnetic resonance imaging (MRI) examinations revealed a left frontal lesion with features suspicious for a tumor. Given the degree of overlap with other pathologic processes, CT and MRI findings failed to provide an unambiguous diagnosis; furthermore, because of the negative cerebrospinal fluid analysis for oligoclonal bands, the absence of other lesions, and the heightened suspicion of neoplasia, the clinicians opted to perform a stereotactic biopsy. Brain specimen analysis did not exclude the possibility of perilesional reactive gliosis and the patient, receiving anitiedemigen therapy, was monthly followed up. In the meanwhile, the second histological opinion of the brain specimen described the absence of pleomorphic glial cells indicating a tumor. These findings were interpreted as destructive inflammatory demyelinating disease and according to the evolution of MRI lesion burden, MS was diagnosed. Conclusion: TDL still remains a problematic entity clinically, radiologically, and sometimes even pathologically. A staged follow-up is necessary, and in our case, it revealed to be the most important attitude to define the nature of the lesion, confirming the classic MS diagnostic criteria of disseminate lesions in time and space. We discuss our findings according to the recent literature. Copyright © 2016 the Author(s). Published by Wolters Kluwer Health, Inc. All.
AUTHOR KEYWORDS: Brain biopsy;  Magnetic resonance spectroscopy;  Multiple sclerosis;  Syringomyelia;  Tumefactive demyelinating lesion;  Tumefactive multiple sclerosis
CORRESPONDENCE ADDRESS: Capasso, R.; Department of Internal Clinical and Experimental Medicine and Surgery, F. Magrassi-A. Lanzara Second University of Naples, Piazza MiragliaItaly; email: dott.ssacapasso@gmail.com
DOCUMENT TYPE: Article

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Jadhao, A.G., Pinelli, C., D'Aniello, B., Tsutsui, K.
Gonadotropin-inhibitory hormone (GnIH) in the amphibian brain and its relationship with the gonadotropin releasing hormone (GnRH) system: An overview
(2017) General and Comparative Endocrinology, 240, pp. 69-76. 
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DOI: 10.1016/j.ygcen.2016.09.006
AFFILIATIONS: Department of Zoology, RTM Nagpur University Campus, Nagpur, MS, India; 
Department of Environmental, Biological, and Pharmaceutical Sciences & Technologies, Second University of Naples, Caserta, Italy; 
Department of Biology, University of Naples “Federico II”, Napoli, Italy; 
Laboratory of Integrative Brain Sciences, Department of Biology and Centre for Medical Life Science, Waseda University, Tokyo, Japan
ABSTRACT: It is well known that the hypothalamic neuropeptide gonadotropin-releasing hormone (GnRH) plays an important role as a primary factor regulating gonadotropin secretion in reproductive processes in vertebrates. The discovery of the presence of a gonadotropin-inhibitory hormone (GnIH) in the brains of birds has further contributed to our understanding of the reproduction control by the brain. GnIH plays a key role in inhibition of reproduction and acts on the pituitary gland and GnRH neurons via a novel G protein-coupled receptor (GPR147). GnIH decreases gonadotropin synthesis and release, thus inhibiting gonadal development and maintenance. The GnRH and GnIH neuronal peptidergic systems are well reported in mammals and birds, but limited information is available regarding their presence and localization in the brains of other vertebrate species, such as reptiles, amphibians and fishes. The aim of this review is to compile and update information on the localization of GnRH and GnIH neuronal systems, with a particular focus on amphibians, summarizing the neuroanatomical distribution of GnIH and GnRH and emphasizing the discovery of GnIH based on RFamide peptides and GnIH orthologous peptides found in other vertebrates and their functional significance. © 2016 Elsevier Inc.
CORRESPONDENCE ADDRESS: Jadhao, A.G.; Department of Zoology, RTM Nagpur University Campus, India; email: agj213@hotmail.com
DOCUMENT TYPE: Article

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Birolo, L., Sacchi, S., Smaldone, G., Molla, G., Leo, G., Caldinelli, L., Pirone, L., Eliometri, P., Di Gaetano, S., Orefice, I., Pedone, E., Pucci, P., Pollegioni, L.
Regulating levels of the neuromodulator d-serine in human brain: structural insight into pLG72 and d-amino acid oxidase interaction
(2016) FEBS Journal, pp. 3353-3370. 
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DOI: 10.1111/febs.13809
AFFILIATIONS: Dipartimento di Scienze Chimiche, Università degli Studi di Napoli Federico II, Napoli, Italy; 
Dipartimento di Biotecnologie e Scienze della Vita, Università degli studi dell'Insubria, Varese, Italy; 
Centro Interuniversitario di Ricerca in Biotecnologie Proteiche “The Protein Factory”, Politecnico di Milano and Università degli studi dell'Insubria, Milano, Italy; 
IRCCS SDN, Napoli, Italy; 
Italian Research National Council, Institute of Biostructures and Bioimaging, Napoli, Italy
ABSTRACT: The human flavoenzyme d-amino acid oxidase (hDAAO) degrades the NMDA-receptor modulator d-serine in the brain. Although hDAAO has been extensively characterized, little is known about its main modulator pLG72, a small protein encoded by the primate-specific gene G72 that has been associated with schizophrenia susceptibility. pLG72 interacts with neosynthesized hDAAO, promoting its inactivation and degradation. In this work, we used low-resolution techniques to characterize the surface topology of the hDAAO–pLG72 complex. By using limited proteolysis coupled to mass spectrometry, we could map the exposed regions in the two proteins after complex formation and highlighted an increased sensitivity to proteolysis of hDAAO in complex with pLG72. Cross-linking experiments by using bis(sulfosuccinimidyl)suberate identified the single covalent bond between T182 in hDAAO and K62 in pLG72. In order to validate the designed mode of interaction, three pLG72 variants incrementally truncated at the C terminus, in addition to a form lacking the 71 N-terminal residues, were produced. All variants were dimeric, folded, and interacted with hDAAO. The strongest decrease in affinity for hDAAO (as well as for the hydrophobic drug chlorpromazine) was apparent for the N-terminally deleted pLG7272–153 form, which lacked K62. On the other hand, eliminating the disordered C-terminal tail yielded a more stable pLG72 protein, improved the binding to hDAAO, although giving lower enzyme inhibition. Elucidation of the mode of hDAAO–pLG72 interaction now makes it possible to design novel molecules that, by targeting the protein complex, can be therapeutically advantageous for diseases related to impairment in d-serine metabolism. © 2016 Federation of European Biochemical Societies
CORRESPONDENCE ADDRESS: Pollegioni, L.; Dipartimento di Biotecnologie e Scienze della Vita, Università degli studi dell'InsubriaItaly; email: loredano.pollegioni@uninsubria.it
DOCUMENT TYPE: Article

Call for abstracts

LE NEUROSCIENZE NELL'AREA NAPOLETANA: PRIMA GIORNATA D'INCONTRO
15 Dicembre 2016 

CEINGE 

Cari colleghi ed amici,

è passato poco più di un anno dal primo incontro del Neapolitan Brain Group che, grazie alla partecipazione di tutti voi, è cresciuto ed inizia ed essere per molti di noi un momento di stimolante interazione culturale nell’ambito delle neuroscienze. A questo punto, un po’ come si fa con le riviste scientifiche ─che nascono con l’amichevole contributo di articoli su invito ma poi devono affrontare la transizione verso l’open submission─ anche noi riteniamo, o dovrei dire speriamo, che i tempi siano maturi per aprire una call for abstracts per il prossimo incontro, denominato: “Le neuroscienze nell’area napoletana: prima giornata d’incontro” che si terrà il 15 Dicembre 2016 presso il CEINGE – Biotecnologie Avanzate, grazie alla disponibilità del suo Presidente Prof. Francesco Salvatore. Questo meeting intende essere in linea con la filosofia che fin dall’inizio ha ispirato l’NBG ovvero promuovere la conoscenza e l’interazione tra tutti coloro che a Napoli e in Campania condividono l’amore per l’affascinante campo delle Neuroscienze. 

Ci auguriamo che l’idea di riunire le realtà scientifiche dell’area napoletana, e, più in generale campana, possa essere uno strumento importante soprattutto per i più giovani (studenti, dottorandi, specializzandi, post-doc)  che dia loro l’opportunità di presentare il proprio lavoro di ricerca alla comunità scientifica di più agevole riferimento. I giovani ricercatori potranno trarre un grande beneficio di crescita dalla discussione che grazie al contributo di tutti ma soprattutto di chi ha un po’ più di esperienza e di chi magari, avendo un background un po’ diverso da chi presenta potrà portarli a riflettere su punti che fino a quel momento non avevano considerato. Soprattutto nell’ottica di estendere ai più giovani l’iniziativa e di fare qualcosa di utile alla loro formazione abbiamo deciso di optare per un formato in linea con quello dei congressi internazionali e che prevede la sottomissione formale di un abstract secondo la form allegata di 250 parole in lingua inglese ed una presentazione, sempre in lingua inglese di 15 minuti inclusa la discussione. Per poter contenere l’incontro entro i limiti della giornata di lavoro, è previsto l’invio di un solo abstract per ciascun Gruppo di Ricerca guidato da un Principal Investigator. La scadenza per la sottomissione è fissata al 15 Novembre 2016. Gli abstracts, scritti seguendo le indicazioni indicate di seguito alla lettera, andranno inviati all’ indirizzo mail: endelgiu@unina.it e saranno revisionati da un Comitato scientifico presieduto dai Proff. Lucio Annunziato, Alessandro Usiello ed Ennio Del Giudice, e dai collaboratori scientifici Carla Lucini, Mauro Cataldi, Elia Di Schiavi) che provvederà ad informare tempestivamente gli autori dell’accettazione delle loro proposte e a preparare il programma definitivo dell’incontro. E’ anche prevista la pubblicazione di un book of abstracts .

Un caro saluto a tutti.

 Ennio Del Giudice,  Carla Lucini,  Elia Di Schiavi,  Mauro Cataldi 

L’abstract deve’essere scritto in inglese. Il nome del file dev’essere il cognome del primo autore. Caratteri:  Times new Roman;  Dimensioni caratteri: 12.

TITOLO (maiuscolo, max 40 parole)

AUTORI (cognome, nome puntato. Sottolineare l’autore che presenterà la comunicazione)

ISTITUZIONI

TESTO  (max 250 parole)

Scopus news

Sestini, S., Perone, R., Domenichetti, S., Mazzeo, C., Massai, V., Rispoli, A., Barbacci, A., Valtancoli, A., Castagnoli, A., Mansi, L.
Brain network underlying the improvement of social functioning in schizophrenic patients after one-year treatment with social skills training
(2016) Current Radiopharmaceuticals, 9 (2), pp. 150-159. 
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84986879745&partnerID=40&md5=fda98dac103365e580df13a33230c6a3

DOI: 10.2174/1874471009999160625110759
AFFILIATIONS: Dept. Diagnostic Imaging, Nuclear Medicine Unit, N.O.P. - S. Stefano, U.S.L. 4, Prato, Italy; 
Dept. of Mental Health, Simple Operative Structure for Adult Mental Health 5 (S.O.S. S.M.A.), A.S.L. 10, Florence, Italy; 
Dept. of Mental Health, Functional Unit for Adult Mental Health (U.F. S.M.A), A.S.L. 10, Florence, Italy; 
Dept. uclear Medicine, Second University of Naples, Italy
ABSTRACT: Purpose: To assess changes in social and neuro-cognition and regional cerebral blood flow (rCBF) in schizophrenic patients with psychotic syndrome treated with Social Skill Training (SST). Methods: 17 patients underwent two high resolution rCBF SPECT at rest before and after a one-year treatment with SST. Patients were assessed using a neuropsychological evaluation (W.A.I.S.-R, T.M.T, Verbal Fluency, W.C.S.T.). SPM8 was used to investigate rCBF changes from the pre- to the post-SST condition and the relationship between rCBF and clinical scores used as covariates of interest. Results: All patients presented with an improvement in social perception, ability to deal with abstract social conventions, rules and judgments about people (Comprehension and Picture Completion sub-tests) and some neuro-cognitive functions sustaining the process of socially relevant information. The main effect of SST was to produce rCBF increases in precuneus, PCC, superior parietal lobules, PMC, pre-SMA, precentral gyrus, dmPFC, dlPFC, vmPFC, OFC (p<0.0001 uncorrected). The SPM analysis showed that Comprehension was supported by PMC, dmPFC, OFC and vmPFC, while the Picture Completion was supported by PMC and dmPFC (p<0.0001). Conclusion: SST in schizophrenic patients improves resting neural activity in cortical areas of the amigdala-based and non-amygdala networks of social brain, including dmPFC and vmPFC, and dlPFC, which are known to be part of default mode and task-positive networks and to be implicated in schizophrenia. © 2016 Bentham Science Publishers.
CORRESPONDENCE ADDRESS: Sestini, S.; Nuclear Medicine Unit, N.O.P. - S. Stefano, U.S.L. 4Italy; email: ssestini@uslcentro.toscana.it
DOCUMENT TYPE: Article
SOURCE: Scopus

Scopus news

Rampino, A., Di Carlo, P., Fazio, L., Ursini, G., Pergola, G., De Virgilio, C., Gadaleta, G., Giordano, G.M., Bertolino, A., Blasi, G.
Association of functional genetic variation in PP2A with prefrontal working memory processing
(2017) Behavioural Brain Research, 316, pp. 125-130. 
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84986000947&partnerID=40&md5=14c6a6081f3495e61240313db1a66a8f

DOI: 10.1016/j.bbr.2016.08.054
AFFILIATIONS: Department of Basic Medical Science, Neuroscience, Sense Organs – University of Bari ‘Aldo Moro’, Piazza Giulio Cesare 11, Bari, Italy; 
Psychiatry Unit – Bari University Hospital, Piazza Giulio Cesare 11, Bari, Italy; 
Lieber Institute for Brain Development, Johns Hopkins University Medical Campus, Baltimore, (MD), United States; 
Department of Bioscience, Biotechnologies and Biopharmaceutics − − University of Bari ‘Aldo Moro’, Via E. Orabona, 4, Bari, Italy; 
University of Naples SUN, Department of Psychiatry, Largo Madonna delle Grazie 1, Naples, Italy
ABSTRACT: Variation in prefrontal dopaminergic signaling mediated by D2 receptor has been implicated in cognitive phenotypes of schizophrenia, including working memory. Molecular cascades downstream of D2 receptor include a cAMP-dependent- and a cAMP-independent-pathway. Protein-Phosphatase-2A (PP2A) is a key partner of D2 receptor in cAMP-independent signaling. This enzyme comprises a regulatory subunit that is coded by PPP2R2B gene. Given the molecular relationship between PP2A and D2 signaling, we hypothesized genetic variation in PPP2R2B affecting mRNA expression of this gene in prefrontal cortex to be associated with prefrontal processing during working memory. In order to probe such a hypothesis we investigated SNPs associated with PPP2R2B expression in two independent samples of human postmortem prefrontal cortex. Then, we tested SNPs for which association was replicated as predictors of prefrontal activity during WM as probed by functional magnetic resonance (fMRI) in a sample of healthy humans. We found that a SNP associated with PPP2R2B expression (rs959627) predicted prefrontal activity during the N-Back working memory task. In particular, individuals carrying rs959627T allele, a condition associated with lower PPP2R2B expression in postmortem prefrontal cortex, showed greater activity in right inferior frontal gyrus (IFG) during N-Back compared to CC subjects. Furthermore, such an activity was negatively correlated with behavioral performance at the task. Consistently with previous studies, these findings suggest reduced right IFG efficiency during working memory processing in rs959627 T-carriers, as indexed by their greater need to activate this brain region in order to achieve similar levels of behavioral proficiency as compared to CC individuals. © 2016 Elsevier B.V.
CORRESPONDENCE ADDRESS: Blasi, G.; Psychiatry Unit – Bari University Hospital, Piazza Giulio Cesare 11, Italy; email: blasi.seppe@gmail.com
DOCUMENT TYPE: Article

Scopus news

Motta, M., Tatti, M., Furlan, F., Celato, A., Di Fruscio, G., Polo, G., Manara, R., Nigro, V., Tartaglia, M., Burlina, A., Salvioli, R.
Clinical, biochemical and molecular characterization of prosaposin deficiency
(2016) Clinical Genetics, 90 (3), pp. 220-229. 
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84983394723&partnerID=40&md5=676dabda308cb3bbda8e40228cffa095

DOI: 10.1111/cge.12753
AFFILIATIONS: Genetics and Rare Diseases Research Division, Ospedale Pediatrico Bambino Gesù, Rome, Italy; 
Department of Haematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy; 
Division of Inherited Metabolic Diseases, University Hospital, Padua, Italy; 
Department of Biochemistry, Biophysics and General Pathology, Second University of Naples, Naples, Italy; 
Telethon Institute of Genetics and Medicine (TIGEM), Naples, Italy
ABSTRACT: Prosaposin (PSAP) deficiency is an ultra-rare, fatal infantile lysosomal storage disorder (LSD) caused by variants in the PSAP gene, with seven subjects reported so far. Here, we provide the clinical, biochemical and molecular characterization of two additional PSAP deficiency cases. Lysoplex, a targeted resequencing approach was utilized to identify the variant in the first patient, while quantification of plasma lysosphingolipids (lysoSLs), assessed by liquid chromatography mass spectrometry (LC-MS/MS) and brain magnetic resonance imaging (MRI), followed by Sanger sequencing allowed to attain diagnosis in the second case. Functional studies were carried out on patients' fibroblast lines to explore the functional impact of variants. The two patients were homozygous for two different truncating PSAP mutations (c.895G>T, p.Glu299*; c.834_835delGA, p.Glu278Aspfs*27). Both variants led to a complete lack of processed transcript. LC-MS/MS and brain MRI analyses consistently provided a distinctive profile in the two children. Quantification of specific plasma lysoSLs revealed elevated levels of globotriaosylsphingosine (LysoGb3) and glucosylsphingosine (GlSph), and accumulation of autophagosomes, due to a decreased autophagic flux, was observed. This report documents the successful use of plasma lysoSLs profiling in the PSAP deficiency diagnosis, as a reliable and informative tool to obtain a preliminary information in infantile cases with complex traits displaying severe neurological signs and visceral involvement. © 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
CORRESPONDENCE ADDRESS: Salvioli, R.; Department of Haematology, Oncology and Molecular Medicine, Istituto Superiore di SanitàItaly; email: rosa.salvioli@iss.it
DOCUMENT TYPE: Article

Iasevoli, F., Laroøi, F., Buonaguro, E.F., Gebhardt, E., Raballo, A.
Can the "connectomic way" provide a link between molecular neurobiology and phenomenological psychopathology? the case of schizophrenia
(2015) Journal of Psychopathology, 21 (4), pp. 323-331. 
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84983156593&partnerID=40&md5=d23d9171687379a678553b70abfb5e44

AFFILIATIONS: Laboratory of Molecular and Translational Psychiatry, Department of Neuroscience, Reproductive and Odontostomatological Sciences, University School of Medicine Federico II, Naples, Italy; 
Outpatient Unit on Treatment Resistant Psychosis, Department of Neuroscience, Reproductive and Odontostomatological Sciences, University School of Medicine Federico II, Naples, Italy; 
Department of Psychology: Cognition and Behaviour, University of Liège, Liège, Belgium; 
Department of Biological and Medical Psychology, University of Bergen, Bergen, Norway; 
Neurosciences, Mental Health and Sensory Functions (NESMOS) Department, Sant'Andrea Hospital, Sapienza University of Rome, Rome, Italy; 
Norwegian Centre for Mental Disorders Research (NORMENT), University of Oslo, Diakonhjemmet Hospital, PB 85 Vinderen, Oslo, Norway
ABSTRACT: Schizophrenia is a severe and complex mental illness whose aetiology remains unknoIasewn. Moreover, changing definitions of the diagnostic criteria of schizophrenia over past decades have not contributed to any substantial progress in terms of deeper pathophysiological understanding of the disease. Nevertheless, to date, significant evidence continues to be accumulated from epidemiologic, genetic and preclinical studies that point to a number of genetic factors that play important roles in the pathophysiology of schizophrenia, especially in terms of disrupted synaptic plasticity molecular processes. Specifically, the most recent approach in human research on schizophrenia is represented by "connectomics" or the study of connectomes, which can be defined as comprehensive maps of connections within an organism's nervous system. Indeed, it has been suggested that schizophrenic pathophysiology might rely on circuit-based dysfunctions that may represent the consequence, on a network scale, of the impairment in synaptic plasticity and neuronal connections that are increasingly found in preclinical molecular research, and that may stem from de novo and/or inherited disease- variants in target genes as well as from aberrant epigenetic mechanisms. On the other hand, circuit-based dysfunctions may underlie the defects in integration of higher-order cognitive functions that characteristically connote schizophrenia patients, and may account for aberrant self-experience which are typically described in phenomenological approaches to the disease. In this paper, we will critically explore the recent advances on molecular, genetic and neuro-imaging research in schizophrenia. Based on these data, we will emphasise the potential of the connectomic framework as an intermediate step between the biological and the phenomenological levels to capture the complexity of schizophrenia manifestations.
CORRESPONDENCE ADDRESS: Raballo, A.; Norwegian Centre for Mental Disorders Research (NORMENT), University of Oslo, Diakonhjemmet Hospital, PB 85 Vinderen, Norway; email: andrea.raballo@medisin.uio.no
DOCUMENT TYPE: Article

Scopus news

Femminella, G.D., Leosco, D., Ferrara, N., Rengo, G.
Adrenergic drugs blockers or enhancers for cognitive decline? What to choose for Alzheimer’s disease patients?
(2016) CNS and Neurological Disorders - Drug Targets, 15 (6), pp. 665-671. 
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84981517805&partnerID=40&md5=5d7501b75b13602b5449932d466a63ce

AFFILIATIONS: Division of Geriatrics, Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy; 
Salvatore Maugeri Foundation, IRCCS, Scientific Institute of Telese Terme, Telese Terme, BN, Italy
ABSTRACT: The adrenergic system has an important role in normal central nervous system function as well as in brain disease. The locus coeruleus, the main source of norepinephrine in brain, is involved in the regulation of learning and memory, reinforcement of sleep-wake cycle and synaptic plasticity. In Alzheimer’s disease, locus coeruleus degeneration is observed early in the course of the disease, years before the onset of clinical cognitive signs, with neurofibrillary detected at the stage of mild cognitive impairment, preceding amyloid deposition. Thus, in the last years, a great interest has grown in evaluating the possibility of central adrenergic system modulation as a therapeutic tool in Alzheimer’s disease. However, evidences do not show univocal results, with some studies suggesting that adrenergic stimulation might be beneficial in Alzheimer’s Disease and some others favoring adrenergic blockade. In this review, we summarize data from both hypothesis and describe the pathophysiological role of the adrenergic system in neurodegeneration. © 2016 Bentham Science Publishers.
CORRESPONDENCE ADDRESS: Rengo, G.; Department of Translational Medical Sciences, University of Naples Federico II, Via Sergio Pansini 5, Italy; email: giuseppe.rengo@unina.it
DOCUMENT TYPE: Article

Scopus news

Vidoni, C., Follo, C., Savino, M., Melone, M.A.B., Isidoro, C.
The Role of Cathepsin D in the Pathogenesis of Human Neurodegenerative Disorders
(2016) Medicinal Research Reviews, 36 (5), pp. 845-870. 
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84981543795&partnerID=40&md5=01ab24566520bf8271425538ffe3a2dc

DOI: 10.1002/med.21394
AFFILIATIONS: Laboratory of Molecular Pathology, Department of Health Sciences, Università del Piemonte Orientale “A. Avogadro,”, Novara, Italy; 
Division of Neurology, Department of Clinic and Experimental Medicine and Surgery, Second University of Naples, Naples, Italy; 
InterUniversity Center for Research in Neurosciences, Second University of Naples, Naples, Italy; 
San Francisco General Hospital, University of California San Francisco, San Francisco, CA, United States
ABSTRACT: In familial neurodegenerative disorders, protein aggregates form continuously because of genetic mutations that drive the synthesis of truncated or unfolded proteins. The oxidative stress imposed by neurotransmitters and environmental neurotoxins constitutes an additional threat to the folding of the proteins and the integrity of organelle membranes in neurons. Failure in degrading such altered materials compromises the function of neurons and eventually leads to neurodegeneration. The lysosomal proteolytic enzyme Cathepsin D is the only aspartic-type protease ubiquitously expressed in all the cells of the human body, and it is expressed at high level in the brain. In general, cathepsin D mediated proteolysis is essential to neuronal cell homeostasis through the degradation of unfolded or oxidized protein aggregates delivered to lysosomes via autophagy or endocytosis. More specifically, many altered neuronal proteins that hallmark neurodegenerative diseases (e.g., the amyloid precursor, α-synuclein, and huntingtin) are physiologic substrates of cathepsin D and would abnormally accumulate if not efficiently degraded by this enzyme. Furthermore, experimental evidence indicates that cathepsin D activity is linked to the metabolism of cholesterol and of glycosaminoglycans, which accounts for its involvement in neuronal plasticity. This review focuses on the unique role of cathepsin D mediated proteolysis in the pathogenesis of human neurodegenerative diseases. © 2016 Wiley Periodicals, Inc.
CORRESPONDENCE ADDRESS: Isidoro, C.; Laboratory of Molecular Pathology, Department of Health Sciences, Università del Piemonte Orientale “A. Avogadro,”Italy; email: ciro.isidoro@med.uniupo.it
DOCUMENT TYPE: Review