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496 results on '"Przedborski, S"'

1. Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy

Author

Obeso, JA, Stamelou, M, Goetz, CG, Poewe, W, Lang, AE, Weintraub, D, Burn, D, Halliday, GM, Bezard, E, Przedborski, S, Lehericy, S, Brooks, DJ, Rothwell, JC, Hallett, M, DeLong, MR, Marras, C, Tanner, CM, Ross, GW, Langston, JW, Klein, C, Bonifati, V, Jankovic, J, Lozano, AM, Deuschl, G, Bergman, H, Tolosa, E, Rodriguez‐Violante, M, Fahn, S, Postuma, RB, Berg, D, Marek, K, Standaert, DG, Surmeier, DJ, Olanow, CW, Kordower, JH, Calabresi, P, Schapira, AHV, and Stoessl, AJ

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Neurodegenerative, Brain Disorders, Parkinson's Disease, Neurological, Anniversaries and Special Events, History, 19th Century, History, 20th Century, History, 21st Century, Humans, Parkinson Disease, Shaking Palsy, Parkinson's disease, years anniversary, Human Movement and Sports Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

This article reviews and summarizes 200 years of Parkinson's disease. It comprises a relevant history of Dr. James Parkinson's himself and what he described accurately and what he missed from today's perspective. Parkinson's disease today is understood as a multietiological condition with uncertain etiopathogenesis. Many advances have occurred regarding pathophysiology and symptomatic treatments, but critically important issues are still pending resolution. Among the latter, the need to modify disease progression is undoubtedly a priority. In sum, this multiple-author article, prepared to commemorate the bicentenary of the shaking palsy, provides a historical state-of-the-art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease. © 2017 International Parkinson and Movement Disorder Society.

Published
2017

2. Molsidomine provides neuroprotection against vincristine-induced peripheral neurotoxicity through soluble guanylyl cyclase activation

Author

Utkina-Sosunova, I, Chiorazzi, A, de Planell-Saguer, M, Li, H, Meregalli, C, Pozzi, E, Carozzi, V, Canta, A, Monza, L, Alberti, P, Fumagalli, G, Karan, C, Moayedi, Y, Przedborski, S, Cavaletti, G, Lotti, F, Utkina-Sosunova, Irina, Chiorazzi, Alessia, de Planell-Saguer, Mariangels, Li, Hai, Meregalli, Cristina, Pozzi, Eleonora, Carozzi, Valentina Alda, Canta, Annalisa, Monza, Laura, Alberti, Paola, Fumagalli, Giulia, Karan, Charles, Moayedi, Yalda, Przedborski, Serge, Cavaletti, Guido, Lotti, Francesco, Utkina-Sosunova, I, Chiorazzi, A, de Planell-Saguer, M, Li, H, Meregalli, C, Pozzi, E, Carozzi, V, Canta, A, Monza, L, Alberti, P, Fumagalli, G, Karan, C, Moayedi, Y, Przedborski, S, Cavaletti, G, Lotti, F, Utkina-Sosunova, Irina, Chiorazzi, Alessia, de Planell-Saguer, Mariangels, Li, Hai, Meregalli, Cristina, Pozzi, Eleonora, Carozzi, Valentina Alda, Canta, Annalisa, Monza, Laura, Alberti, Paola, Fumagalli, Giulia, Karan, Charles, Moayedi, Yalda, Przedborski, Serge, Cavaletti, Guido, and Lotti, Francesco

Abstract

Peripheral neurotoxicity is a dose-limiting adverse reaction of primary frontline chemotherapeutic agents, including vincristine. Neuropathy can be so disabling that patients drop out of potentially curative therapy, negatively impacting cancer prognosis. The hallmark of vincristine neurotoxicity is axonopathy, yet its underpinning mechanisms remain uncertain. We developed a comprehensive drug discovery platform to identify neuroprotective agents against vincristine-induced neurotoxicity. Among the hits identified, SIN-1-an active metabolite of molsidomine-prevents vincristine-induced axonopathy in both motor and sensory neurons without compromising vincristine anticancer efficacy. Mechanistically, we found that SIN-1's neuroprotective effect is mediated by activating soluble guanylyl cyclase. We modeled vincristine-induced peripheral neurotoxicity in rats to determine molsidomine therapeutic potential in vivo. Vincristine administration induced severe nerve damage and mechanical hypersensitivity that were attenuated by concomitant treatment with molsidomine. This study provides evidence of the neuroprotective properties of molsidomine and warrants further investigations of this drug as a therapy for vincristine-induced peripheral neurotoxicity.

Published
2024

3. Depletion of Mettl3 in cholinergic neurons causes adult-onset neuromuscular degeneration

Author

Dermentzaki, G, Furlan, M, Tanaka, I, Leonardi, T, Rinchetti, P, Passos, P, Bastos, A, Ayala, Y, Hanna, J, Przedborski, S, Bonanomi, D, Pelizzola, M, Lotti, F, Dermentzaki, Georgia, Furlan, Mattia, Tanaka, Iris, Leonardi, Tommaso, Rinchetti, Paola, Passos, Patricia M S, Bastos, Alliny, Ayala, Yuna M, Hanna, Jacob H, Przedborski, Serge, Bonanomi, Dario, Pelizzola, Mattia, Lotti, Francesco, Dermentzaki, G, Furlan, M, Tanaka, I, Leonardi, T, Rinchetti, P, Passos, P, Bastos, A, Ayala, Y, Hanna, J, Przedborski, S, Bonanomi, D, Pelizzola, M, Lotti, F, Dermentzaki, Georgia, Furlan, Mattia, Tanaka, Iris, Leonardi, Tommaso, Rinchetti, Paola, Passos, Patricia M S, Bastos, Alliny, Ayala, Yuna M, Hanna, Jacob H, Przedborski, Serge, Bonanomi, Dario, Pelizzola, Mattia, and Lotti, Francesco

Abstract

Motor neuron (MN) demise is a hallmark of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Post-transcriptional gene regulation can control RNA's fate, and defects in RNA processing are critical determinants of MN degeneration. N6-methyladenosine (m6A) is a post-transcriptional RNA modification that controls diverse aspects of RNA metabolism. To assess the m6A requirement in MNs, we depleted the m6A methyltransferase-like 3 (METTL3) in cells and mice. METTL3 depletion in embryonic stem cell-derived MNs has profound and selective effects on survival and neurite outgrowth. Mice with cholinergic neuron-specific METTL3 depletion display a progressive decline in motor behavior, accompanied by MN loss and muscle denervation, culminating in paralysis and death. Reader proteins convey m6A effects, and their silencing phenocopies METTL3 depletion. Among the m6A targets, we identified transactive response DNA-binding protein 43 (TDP-43) and discovered that its expression is under epitranscriptomic control. Thus, impaired m6A signaling disrupts MN homeostasis and triggers neurodegeneration conceivably through TDP-43 deregulation.

Published
2024

5. Resistance of SOD-Transgenic Mice to Oxidative Stress

Author

Epstein, C. J., Chan, P. H., Cadet, J. L., Carlson, E., Chen, S., Chu, L., Fahn, S., Jackson-Lewis, V., Kinouchi, H., Kostic, V., Kujirai, K., Mizui, A., Naini, A., Przedborski, S., Yang, G., Christen, Yves, editor, and Gage, Fred H., editor

Published
1992
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7. Molsidomide provides neuroprotection against vincristine-induced peripheral neurotoxicity

Author

Lotti, F, Utkina Sosunova, I, Chiorazzi, A, Carozzi, VA, Canta, A, Monza, L, Alberti, P, Fumagalli, G, Przedborski, S, Cavaletti, G, Lotti, F, Utkina Sosunova, I, Chiorazzi, A, Carozzi, V, Canta, A, Monza, L, Alberti, P, Fumagalli, G, Przedborski, S, and Cavaletti, G

Subjects
axonal biology, pre-clinical studies, pain, axonal regeneration
Abstract

Peripheral neuropathy is the principal dose-limiting adverse reaction of the major frontline chemotherapeutic agents. Neuropathy can be so disabling that many patients will drop out of potentially curative therapy, negatively impacting cancer prognosis. Chemotherapy-induced peripheral neuropathy (CIPN) is refractory to treatment and persists in about 50% of cancer survivors limiting their quality of life. Vincristine is highly active, but its use is limited by the severe neurotoxicity leading to autonomic, sensory and motor impairment. The hallmark of vincristine peripheral neurotoxicity is axonopathy. Yet the underpinning mechanisms of vincristine-induced axonopathy remains uncertain. We hypothesize that agents preventing vincristine-induced axonopathy will effectively mitigate CIPN symptoms, hence improving cancer treatment outcomes and survivors’ quality of life. Based on this premise, we developed a comprehensive drug discovery pipeline to identify small molecules with neuroprotective activity against vincristine-induced axon degeneration. Among the hits identified, SIN-1 – an active metabolite of molsidomine (Covaryl) – prevents VCR-induced axon loss in both motor and sensory neurons, and it does so without compromising vincristine anti-cancer potency. To determine the neuroprotective effect of molsidomine, we used an extensively validated rat model of vincristine-induced peripheral neuropathy. Vincristine (0.2mg/kg/week) was administered via the tail vein for 4 weeks and molsidomine (10mg/kg/day or 20mg/kg/day) was administered orally for 4 weeks, starting the first day of vincristine treatment. As expected, the selected schedule of vincristine administration induced severe sensory and motor nerve damage. Importantly, vincristine-treated rats showed a significant decrease in the sensory threshold determined by the dynamic test that was prevented by molsidomine administration in a dose-dependent manner. A similar protective effect of molsidomine was evident on digital nerve amplitude and velocity. This study provides preliminary evidence of the neuroprotective properties of molsidomine and opens the way to further investigations of this drug as a therapeutic agent to prevent vincristine-induced peripheral neuropathy.

Published
2019

14. Early development of levodopa-induced dyskinesias and response fluctuations in young-onset Parkinson's disease

Author

Kostic, V., Przedborski, S., Flaster, E., and Sternic, N.

Subjects
Parkinsonism -- Drug therapy, Tardive dyskinesia -- Causes of, Parkinsonism -- Demographic aspects, Dopa -- Adverse and side effects, Movement disorders -- Causes of, Health, Psychology and mental health
Abstract

Parkinson's disease generally affects aging patients, but it may occur in younger individuals as well. There is some controversy, however, about what significance the age of onset might have in determining the course of the disease and the prognosis. At least part of the difficulty in determining the clinical importance of age of onset involves the relatively small number of younger patients available for study and the difficulties in assigning an appropriate comparison group of older Parkinson's patients. For this reason, a study was conducted in a large neurology practice which permitted the evaluation of 25 patients with young-onset Parkinson's disease and the careful matching of 25 controls (with older-onset disease). The young-onset patients developed signs of Parkinson's disease prior to the age of 40 years; the 25 control subjects were matched for comparable duration of disease, duration of treatment with levodopa, and a comparable stage of disease. The patients in the two groups had Parkinson's disease for an average of 9.1 years and had been treated with levodopa for an average of 7.3 years. When comparisons were made between the two groups it was found that the patients with younger-onset disease had a significantly greater frequency of dyskinesias, or movement abnormalities, induced by the levodopa treatment than the patients with older-onset disease. After five years of levodopa treatment, 96 percent of the young-onset patients had developed dyskinesias in contrast with 64 percent of the older patients. Furthermore, fluctuations in the response to levodopa were more common among the younger-onset patients; after five years of treatment, 80 percent of the younger patients experienced response fluctuations, compared with 44 percent of the older-onset patients. The data also indicate that the younger-onset Parkinson's patients tended to develop dyskinesias and response fluctuations sooner after the initiation of levodopa therapy than older-onset patients. These results suggest that it may be advisable to delay the use of levodopa as long as possible in patients with young-onset Parkinson's disease. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

15. Molsidomine reduces the severity of Vincristine-induced peripheral neurotoxicity in rats

Author

Chiorazzi, A., Carozzi, V., Paola Alberti, Canta, A., Meregalli, C., Fumagalli, G., Monza, L., Pozzi, E., Oggioni, N., Utkina-Sosunova, I., Przedborski, S., Cavaletti, G., Lotti, F., Chiorazzi, A, Carozzi, V, Alberti, P, Canta, A, Meregalli, C, Fumagalli, G, Monza, L, Pozzi, E, Oggioni, N, Utkina-Sosunova, I, Przedborsk, S, Cavaletti, G, and Lotti, F

Subjects
Peripheral Neurotoxicity, Animal models, Neuroprotection, Translational Medicine, Cancer, Neuropathy, Vincristine
Published
2019

16. Hemiparkinsonism-hemiatrophy syndrome: clinical and radiologic features

Author

Giladi, N., Burke, R.E., Kostic, V., Przedborski, S., Gordon, M., Hunt, A., and Fahn, S.

Subjects
Parkinsonism -- Physiological aspects, Atrophy -- Causes of, Health, Psychology and mental health
Abstract

Hemiparkinsonism-hemiatrophy syndrome is parkinsonian symptoms limited to half the body, with atrophy on the same side of the body or brain atrophy on the opposite side. This rare condition generally begins earlier in life than most forms of parkinsonism. While the syndrome was defined on the basis of purely clinical symptoms, the advent of modern imaging techniques has provided new insights into the pathological picture of hemiparkinsonism-hemiatrophy syndrome. The authors reviewed 11 cases of hemiparkinsonism-hemiatrophy syndrome in 2 women and 9 men. The average age of onset of the syndrome in these patients was 38.1 years; there was no family history of parkinsonism among these patients and only two patients had any history of head trauma. Six of the patients had body hemiatrophy and contralateral (opposite side) brain atrophy, four had only body hemiatrophy, and one patient had only brain hemiatrophy in addition to the hemiparkinsonism. In seven patients the affected side was the dominant side and in four the affected side was nondominant. No correlation could be found between the degrees of brain hemiatrophy and body hemiatrophy. Five of the patients developed bilateral disease as their condition progressed. This observation, which has been made in previous reports of hemiparkinsonism, suggests that both sides of the brain may be affected, but one side has a considerable head start in degenerating. One common hypothesis of the etiology of hemiparkinsonism-hemiatrophy is that the condition arises from perinatal asphyxia (insufficient oxygenation in the period shortly before to shortly after birth). It is not easy, however, to explain the long delay between the initial brain insult and the development of symptoms. One possibility, however, is that the perinatal insult carries the brain close to the edge of parkinsonian symptoms. It is known that significant destruction of neurons in the substantia nigra must take place before parkinsonian symptoms appear. If the perinatal insult comes close to the threshold, then a slight loss of neurons, which would be uneventful in a normal individual, might carry these patients over the threshold and result in neurological symptoms. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

19. Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy

Author

Obeso, J.A. Stamelou, M. Goetz, C.G. Poewe, W. Lang, A.E. Weintraub, D. Burn, D. Halliday, G.M. Bezard, E. Przedborski, S. Lehericy, S. Brooks, D.J. Rothwell, J.C. Hallett, M. DeLong, M.R. Marras, C. Tanner, C.M. Ross, G.W. Langston, J.W. Klein, C. Bonifati, V. Jankovic, J. Lozano, A.M. Deuschl, G. Bergman, H. Tolosa, E. Rodriguez-Violante, M. Fahn, S. Postuma, R.B. Berg, D. Marek, K. Standaert, D.G. Surmeier, D.J. Olanow, C.W. Kordower, J.H. Calabresi, P. Schapira, A.H.V. Stoessl, A.J.

Abstract

This article reviews and summarizes 200 years of Parkinson's disease. It comprises a relevant history of Dr. James Parkinson's himself and what he described accurately and what he missed from today's perspective. Parkinson's disease today is understood as a multietiological condition with uncertain etiopathogenesis. Many advances have occurred regarding pathophysiology and symptomatic treatments, but critically important issues are still pending resolution. Among the latter, the need to modify disease progression is undoubtedly a priority. In sum, this multiple-author article, prepared to commemorate the bicentenary of the shaking palsy, provides a historical state-of-the-art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease. © 2017 International Parkinson and Movement Disorder Society. © 2017 International Parkinson and Movement Disorder Society

Published
2017

20. Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy

Author

Obeso, J.A., Stamelou, M., Goetz, C.G., Poewe, W., Lang, A.E., Weintraub, D., Burn, D., Halliday, G.M., Bezard, E., Przedborski, S., Lehericy, S., Brooks, D.J., Rothwell, J.C., Hallett, M., DeLong, M.R., Marras, C., Tanner, C.M., Ross, G.W., Langston, J.W., Klein, C., Bonifati, V., Jankovic, J., Lozano, A.M., Deuschl, G., Bergman, H., Tolosa, E., Rodriguez-Violante, M., Fahn, S., Postuma, R.B., Berg, D., Marek, K., Standaert, D.G., Surmeier, D.J., Olanow, C.W., Kordower, J.H., Calabresi, P., Schapira, A.H.V., Stoessl, A.J., and Clinical Genetics

Subjects
History, 200 years anniversary, Parkinson's disease, Shaking Palsy, Anniversaries and Special Events, History, 19th Century, History, 20th Century, History, 21st Century, Humans, Parkinson Disease, Neurology, Neurology (clinical), Clinical Sciences, Review, Neurodegenerative, Article, Journal Article, 19th Century, Neurology & Neurosurgery, Neurosciences, Human Movement and Sports Sciences, 21st Century, Brain Disorders, 20th Century, years anniversary, Neurological
Abstract

This article reviews and summarizes 200 years of Parkinson's disease. It comprises a relevant history of Dr. James Parkinson's himself and what he described accurately and what he missed from today's perspective. Parkinson's disease today is understood as a multietiological condition with uncertain etiopathogenesis. Many advances have occurred regarding pathophysiology and symptomatic treatments, but critically important issues are still pending resolution. Among the latter, the need to modify disease progression is undoubtedly a priority. In sum, this multiple-author article, prepared to commemorate the bicentenary of the shaking palsy, provides a historical state-of-the-art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease. © 2017 International Parkinson and Movement Disorder Society.

Published
2017
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25. Creation of an open-access, mutation-defined fibroblast resource for neurological disease research

Author

Wray, S, Self, M, Lewis, PA, Taanman, JW, Ryan, NS, Mahoney, CJ, Liang, Y, Devine, MJ, Sheerin, UM, Houlden, H, Morris, HR, Healy, D, Marti-Masso, JF, Preza, E, Barker, S, Sutherland, M, Corriveau, RA, D'Andrea, M, Schapira, AHV, Uitti, RJ, Guttman, M, Opala, G, Jasinska-Myga, B, Puschmann, A, Nilsson, C, Espay, AJ, Slawek, J, Gutmann, L, Boeve, BF, Boylan, K, Jon Stoessl, A, Ross, OA, Maragakis, NJ, Van Gerpen, J, Gerstenhaber, M, Gwinn, K, Dawson, TM, Isacson, O, Marder, KS, Clark, LN, Przedborski, SE, Finkbeiner, S, Rothstein, JD, Wszolek, ZK, Rossor, MN, Hardy, J, Gusella, JF, MacDonald, ME, Wheeler, VC, Ross, CA, Akimov, S, Arjomand, J, Thompson, LM, King, A, Hermanowicz, N, Winokur, S, Svendsen, CN, Mattis, V, Onorati, M, Cattaneo, E, Allen, ND, Kemp, PJ, Kim, KS, Przedborski, S, Feng, J, Lee, VMY, Trojanowski, JQ, James Surmeier, D, Henderson, CE, Maniatis, T, Eggan, K, and Cudowicz, ME

Abstract

Our understanding of the molecular mechanisms of many neurological disorders has been greatly enhanced by the discovery of mutations in genes linked to familial forms of these diseases. These have facilitated the generation of cell and animal models that can be used to understand the underlying molecular pathology. Recently, there has been a surge of interest in the use of patient-derived cells, due to the development of induced pluripotent stem cells and their subsequent differentiation into neurons and glia. Access to patient cell lines carrying the relevant mutations is a limiting factor for many centres wishing to pursue this research. We have therefore generated an open-access collection of fibroblast lines from patients carrying mutations linked to neurological disease. These cell lines have been deposited in the National Institute for Neurological Disorders and Stroke (NINDS) Repository at the Coriell Institute for Medical Research and can be requested by any research group for use in in vitro disease modelling. There are currently 71 mutation-defined cell lines available for request from a wide range of neurological disorders and this collection will be continually expanded. This represents a significant resource that will advance the use of patient cells as disease models by the scientific community.

Published
2012
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26. Guidelines for the use and interpretation of assays for monitoring autophagy

Author

Klionsky, D.J. Abdalla, F.C. Abeliovich, H. Abraham, R.T. Acevedo-Arozena, A. Adeli, K. Agholme, L. Agnello, M. Agostinis, P. Aguirre-Ghiso, J.A. Ahn, H.J. Ait-Mohamed, O. Ait-Si-Ali, S. Akematsu, T. Akira, S. Al-Younes, H.M. Al-Zeer, M.A. Albert, M.L. Albin, R.L. Alegre-Abarrategui, J. Aleo, M.F. Alirezaei, M. Almasan, A. Almonte-Becerril, M. Amano, A. Amaravadi, R. Amarnath, S. Amer, A.O. Andrieu-Abadie, N. Anantharam, V. Ann, D.K. Anoopkumar-Dukie, S. Aoki, H. Apostolova, N. Arancia, G. Aris, J.P. Asanuma, K. Asare, N.Y.O. Ashida, H. Askanas, V. Askew, D.S. Auberger, P. Baba, M. Backues, S.K. Baehrecke, E.H. Bahr, B.A. Bai, X.-Y. Bailly, Y. Baiocchi, R. Baldini, G. Balduini, W. Ballabio, A. Bamber, B.A. Bampton, E.T.W. Bánhegyi, G. Bartholomew, C.R. Bassham, D.C. Bast Jr., R.C. Batoko, H. Bay, B.-H. Beau, I. Béchet, D.M. Begley, T.J. Behl, C. Behrends, C. Bekri, S. Bellaire, B. Bendall, L.J. Benetti, L. Berliocchi, L. Bernardi, H. Bernassola, F. Besteiro, S. Bhatia-Kissova, I. Bi, X. Biard-Piechaczyk, M. Blum, J.S. Boise, L.H. Bonaldo, P. Boone, D.L. Bornhauser, B.C. Bortoluci, K.R. Bossis, I. Bost, F. Bourquin, J.-P. Boya, P. Boyer-Guittaut, M. Bozhkov, P.V. Brady, N.R. Brancolini, C. Brech, A. Brenman, J.E. Brennand, A. Bresnick, E.H. Brest, P. Bridges, D. Bristol, M.L. Brookes, P.S. Brown, E.J. Brumell, J.H. Brunetti-Pierri, N. Brunk, U.T. Bulman, D.E. Bultman, S.J. Bultynck, G. Burbulla, L.F. Bursch, W. Butchar, J.P. Buzgariu, W. Bydlowski, S.P. Cadwell, K. Cahová, M. Cai, D. Cai, J. Cai, Q. Calabretta, B. Calvo-Garrido, J. Camougrand, N. Campanella, M. Campos-Salinas, J. Candi, E. Cao, L. Caplan, A.B. Carding, S.R. Cardoso, S.M. Carew, J.S. Carlin, C.R. Carmignac, V. Carneiro, L.A.M. Carra, S. Caruso, R.A. Casari, G. Casas, C. Castino, R. Cebollero, E. Cecconi, F. Celli, J. Chaachouay, H. Chae, H.-J. Chai, C.-Y. Chan, D.C. Chan, E.Y. Chang, R.C.-C. Che, C.-M. Chen, C.-C. Chen, G.-C. Chen, G.-Q. Chen, M. Chen, Q. Chen, S.S.-L. Chen, W. Chen, X. Chen, X. Chen, X. Chen, Y.-G. Chen, Y. Chen, Y. Chen, Y.-J. Chen, Z. Cheng, A. Cheng, C.H.K. Cheng, Y. Cheong, H. Cheong, J.-H. Cherry, S. Chess-Williams, R. Cheung, Z.H. Chevet, E. Chiang, H.-L. Chiarelli, R. Chiba, T. Chin, L.-S. Chiou, S.-H. Chisari, F.V. Cho, C.H. Cho, D.-H. Choi, A.M.K. Choi, D. Choi, K.S. Choi, M.E. Chouaib, S. Choubey, D. Choubey, V. Chu, C.T. Chuang, T.-H. Chueh, S.-H. Chun, T. Chwae, Y.-J. Chye, M.-L. Ciarcia, R. Ciriolo, M.R. Clague, M.J. Clark, R.S.B. Clarke, P.G.H. Clarke, R. Codogno, P. Coller, H.A. Colombo, M.I. Comincini, S. Condello, M. Condorelli, F. Cookson, M.R. Coombs, G.H. Coppens, I. Corbalan, R. Cossart, P. Costelli, P. Costes, S. Coto-Montes, A. Couve, E. Coxon, F.P. Cregg, J.M. Crespo, J.L. Cronjé, M.J. Cuervo, A.M. Cullen, J.J. Czaja, M.J. D'Amelio, M. Darfeuille-Michaud, A. Davids, L.M. Davies, F.E. De Felici, M. De Groot, J.F. De Haan, C.A.M. De Martino, L. De Milito, A. De Tata, V. Debnath, J. Degterev, A. Dehay, B. Delbridge, L.M.D. Demarchi, F. Deng, Y.Z. Dengjel, J. Dent, P. Denton, D. Deretic, V. Desai, S.D. Devenish, R.J. Di Gioacchino, M. Di Paolo, G. Di Pietro, C. Díaz-Araya, G. Díaz-Laviada, I. Diaz-Meco, M.T. Diaz-Nido, J. Dikic, I. Dinesh-Kumar, S.P. Ding, W.-X. Distelhorst, C.W. Diwan, A. Djavaheri-Mergny, M. Dokudovskaya, S. Dong, Z. Dorsey, F.C. Dosenko, V. Dowling, J.J. Doxsey, S. Dreux, M. Drew, M.E. Duan, Q. Duchosal, M.A. Duff, K. Dugail, I. Durbeej, M. Duszenko, M. Edelstein, C.L. Edinger, A.L. Egea, G. Eichinger, L. Eissa, N.T. Ekmekcioglu, S. El-Deiry, W.S. Elazar, Z. Elgendy, M. Ellerby, L.M. Er Eng, K. Engelbrecht, A.-M. Engelender, S. Erenpreisa, J. Escalante, R. Esclatine, A. Eskelinen, E.-L. Espert, L. Espina, V. Fan, H. Fan, J. Fan, Q.-W. Fan, Z. Fang, S. Fang, Y. Fanto, M. Fanzani, A. Farkas, T. Farré, J.-C. Faure, M. Fechheimer, M. Feng, C.G. Feng, J. Feng, Q. Feng, Y. Fésüs, L. Feuer, R. Figueiredo-Pereira, M.E. Fimia, G.M. Fingar, D.C. Finkbeiner, S. Finkel, T. Finley, K.D. Fiorito, F. Fisher, E.A. Fisher, P.B. Flajolet, M. Florez-McClure, M.L. Florio, S. Fon, E.A. Fornai, F. Fortunato, F. Fotedar, R. Fowler, D.H. Fox, H.S. Franco, R. Frankel, L.B. Fransen, M. Fuentes, J.M. Fueyo, J. Fujii, J. Fujisaki, K. Fujita, E. Fukuda, M. Furukawa, R.H. Gaestel, M. Gailly, P. Gajewska, M. Galliot, B. Galy, V. Ganesh, S. Ganetzky, B. Ganley, I.G. Gao, F.-B. Gao, G.F. Gao, J. Garcia, L. Garcia-Manero, G. Garcia-Marcos, M. Garmyn, M. Gartel, A.L. Gatti, E. Gautel, M. Gawriluk, T.R. Gegg, M.E. Geng, J. Germain, M. Gestwicki, J.E. Gewirtz, D.A. Ghavami, S. Ghosh, P. Giammarioli, A.M. Giatromanolaki, A.N. Gibson, S.B. Gilkerson, R.W. Ginger, M.L. Ginsberg, H.N. Golab, J. Goligorsky, M.S. Golstein, P. Gomez-Manzano, C. Goncu, E. Gongora, C. Gonzalez, C.D. Gonzalez, R. González-Estévez, C. González-Polo, R.A. Gonzalez-Rey, E. Gorbunov, N.V. Gorski, S. Goruppi, S. Gottlieb, R.A. Gozuacik, D. Granato, G.E. Grant, G.D. Green, K.N. Gregorc, A. Gros, F. Grose, C. Grunt, T.W. Gual, P. 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Abstract

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field. © 2012 Landes Bioscience.

Published
2012

27. Measurement of the bottom-strange meson mixing phase in the full CDF data set

Author

Aaltonen, T., Alvarez, González, Amerio, B., Amidei, S., Anastassov, D., Annovi, A., Antos, A., Apollinari, J., Appel, G., J. A., Arisawa, Artikov, T., Asaadi, A., Ashmanskas, J., Auerbach, W., Aurisano, B., Azfar, A., Badgett, F., Bae, W., Barbaro, Galtieri, Barnes, A., V. E., Barnett, B. A., Barria, Bartos, P., Bauce, P., Bedeschi, M., Behari, F., Bellettini, S., Bellinger, G., Benjamin, J., Beretvas, D., Bhatti, A., Bisello, A., Bizjak, D., Bland, I., K. R., Blumenfeld, Bocci, B., Bodek, A., Bortoletto, A., Boudreau, D., Boveia, J., Brigliadori, A., Bromberg, L., Brucken, C., Budagov, E., Budd, J., H. S., Burkett, Busetto, K., Bussey, G., Buzatu, P., Calamba, A., Calancha, A., Camarda, C., Campanelli, S., Campbell, M., Canelli, M., Carls, F., Carlsmith, B., Carosi, D., Carrillo, R., Carron, S., Casal, S., Casarsa, B., Castro, M., Catastini, A., Cauz, P., Cavaliere, D., Cavalli, Sforza, Cerri, M., Cerrito, A., Chen, L., Y. C., Chertok, Chiarelli, M., Chlachidze, G., Chlebana, G., Cho, F., Chokheli, K., Chung, D., W. H., Chung, Y. S., Ciocci, M. A., Clark, Clarke, A., Compostella, C., Convery, G., M. E., Conway, Corbo, J., Cordelli, M., Cox, M., C. A., Cox, D. J., Crescioli, Cuevas, F., Culbertson, J., Dagenhart, R., D'Ascenzo, D., Datta, N., Barbaro, De, Dell'Orso, Mauro, Demortier, M., Deninno, L., Devoto, M., D'Errico, F., Canto, Di, Ruzza, Di, Dittmann, B., J. R., D'Onofrio, Donati, Simone, Dong, P., Dorigo, M., Dorigo, T., Ebina, K., Elagin, A., Eppig, A., Erbacher, R., Errede, S., Ershaidat, N., Eusebi, R., Farrington, S., Feindt, M., Fernandez, J. P., Field, R., Flanagan, G., Forrest, R., Frank, M. J., Franklin, M., Freeman, J. C., Funakoshi, Y., Furic, I., Gallinaro, M., Garcia, J. E., Garfinkel, A. F., Garosi, P., Gerberich, H., Gerchtein, E., Giagu, S., Giakoumopoulou, V., Giannetti, P., Gibson, K., Ginsburg, C. M., Giokaris, N., Giromini, P., Giurgiu, G., Glagolev, V., Glenzinski, D., Gold, M., Goldin, D., Goldschmidt, N., Golossanov, A., Gomez, G., Gomez, Ceballos, Goncharov, G., González, M., Gorelov, O., Goshaw, I., A. T., Goulianos, Grillo, K., Grinstein, L., Grosso, Pilcher, Group, C., R. C., Guimaraes Da Costa, Hahn, J., S. R., Halkiadakis, Hamaguchi, E., Han, A., J. Y., Happacher, Hara, F., Hare, K., Hare, D., Harr, M., R. F., Hatakeyama, Hays, K., Heck, C., Heinrich, M., Herndon, J., Hewamanage, M., Hocker, S., Hopkins, A., Horn, W., Hou, D., Hughes, S., R. E., Hurwitz, Husemann, M., Hussain, U., Hussein, N., Huston, M., Introzzi, J., Iori, G., Ivanov, M., James, A., Jang, E., Jayatilaka, D., Jeon, B., E. J., Jindariani, Jones, S., Joo, M., K. K., Jun, S. Y., Junk, T. R., Kamon, Karchin, T., P. E., Kasmi, Kato, A., Ketchum, Y., Keung, W., Khotilovich, J., Kilminster, V., Kim, B., D. H., Kim, H. S., Kim, J. E., Kim, M. J., Kim, S. B., Kim, S. H., Kim, Y. K., Kim, Y. J., Kimura, Kirby, N., Klimenko, M., Knoepfel, S., Kondo, K., Kong, K., D. J., Konigsberg, Kotwal, J., A. V., Kreps, Kroll, M., Krop, J., Kruse, D., Krutelyov, M., Kuhr, V., Kurata, T., Kwang, M., Laasanen, S., A. T., Lami, Lammel, S., Lancaster, S., Lander, M., R. L., Lannon, Lath, K., Latino, A., Lecompte, G., Lee, T., Lee, E., H. S., Lee, J. S., Lee, S. W., Leo, Leone, S., Lewis, S., J. D., Limosani, Lin, A., C. J., Lindgren, Lipeles, M., Lister, E., Litvintsev, A., D. O., Liu, Liu, C., Liu, H., Liu, Q., Lockwitz, T., Loginov, S., Lucchesi, A., Lueck, D., Lujan, J., Lukens, P., Lungu, P., Lys, G., Lysak, J., Madrak, R., Maeshima, R., Maestro, K., Malik, P., Manca, S., Manousakis, Katsikakis, Margaroli, A., Marino, F., Martínez, C., Mastrandrea, M., Matera, P., Mattson, K., M. E., Mazzacane, Mazzanti, A., Mcfarland, P., K. S., Mcintyre, Mcnulty, P., Mehta, R., Mehtala, A., Mesropian, P., Miao, C., Mietlicki, T., Mitra, D., Miyake, A., Moed, H., Moggi, S., Mondragon, N., M. N., Moon, C. S., Moore, Morello, R., M. J., Morlock, Movilla, Fernandez, Mukherjee, P., Muller, A., Murat, T., Mussini, P., Nachtman, M., Nagai, J., Naganoma, Y., Nakano, J., Napier, I., Nett, A., Neu, J., Neubauer, C., M. S., Nielsen, Nodulman, J., Noh, L., S. Y., Norniella, Oakes, O., Oh, L., S. H., Oh, Y. D., Oksuzian, Okusawa, I., Orava, T., Ortolan, R., Pagan, Griso, Pagliarone, S., Palencia, C., Papadimitriou, E., Paramonov, V., A. A., Patrick, Pauletta, J., Paulini, G., Paus, M., Pellett, C., D. E., Penzo, Phillips, A., T. J., Piacentino, Pianori, G., Pilot, E., Pitts, J., Plager, K., Pondrom, C., Poprocki, L., Potamianos, S., Prokoshin, K., Pranko, F., Ptohos, A., Punzi, Giovanni, Rahaman, G., Ramakrishnan, A., Ranjan, V., Redondo, N., Renton, I., Rescigno, P., Riddick, M., Rimondi, T., Ristori, F., Robson, L., Rodrigo, A., Rodriguez, T., Rogers, T., Rolli, E., Roser, S., Ruffini, R., Ruiz, F., Russ, A., Rusu, J., Safonov, V., Sakumoto, A., W. K., Sakurai, Santi, Y., Sato, L., Saveliev, K., Savoy, Navarro, Schlabach, A., Schmidt, P., Schmidt, A., E. E., Schwarz, Scodellaro, T., Scribano, L., Scuri, A., Seidel, F., Seiya, S., Semenov, Y., Sforza, A., Shalhout, F., S. Z., Shears, Shepard, T., P. F., Shimojima, Shochet, M., Shreyber, Tecker, Simonenko, I., Sinervo, A., Sliwa, P., Smith, K., J. R., Snider, F. D., Soha, Sorin, A., Song, V., Squillacioti, H., Stancari, P., Denis, S. t., Stelzer, R., Stelzer, Chilton, Stentz, O., Strologas, D., Strycker, J., G. L., Sudo, Sukhanov, Y., Suslov, A., Takemasa, I., Takeuchi, K., Tang, Y., Tecchio, J., Teng, M., P. K., Thom, Thome, J., Thompson, J., G. A., Thomson, Toback, E., Tokar, D., Tollefson, S., Tomura, K., Tonelli, T., Torre, D., Torretta, S., Totaro, D., Trovato, P., Ukegawa, M., Uozumi, F., Varganov, S., Vázquez, A., Velev, F., Vellidis, G., Vidal, C., Vila, M., Vilar, I., Vizán, R., Vogel, J., Volpi, M., Wagner, G., Wagner, P., R. L., Wakisaka, Wallny, T., Wang, R., S. M., Warburton, Waters, A., Wester, D., W. C., Whiteson, Wicklund, D., A. B., Wicklund, Wilbur, E., Wick, S., Williams, F., H. H., Wilson, J. S., Wilson, Winer, P., B. L., Wittich, Wolbers, P., Wolfe, S., Wright, H., Wu, T., Wu, X., Yamamoto, Z., Yamato, K., Yang, D., Yang, T., U. K., Yang, Y. C., Yao, W. M., Yeh, G. P., Yi, Yoh, K., Yorita, J., Yoshida, K., Yu, T., G. B., Yu, Yu, I., S. S., Yun, J. C., Zanetti, Zeng, A., Zhou, Y., Zucchelli, C., Jy, S., Koh, Yh, Koike, M, Komatsu, M, Kominami, E, Kong, Hj, Kong, Wj, Korolchuk, Vi, Kotake, Y, Koukourakis, Mi, Kouri Flores JB, Kovács, Al, Kraft, C, Krainc, D, Krämer, H, Kretz Remy, C, Krichevsky, Am, Kroemer, G, Krüger, R, Krut, O, Ktistakis, Nt, Kuan, Cy, Kucharczyk, R, Kumar, A, Kumar, R, Kumar, S, Kundu, M, Kung, Hj, Kurz, T, Kwon, Hj, La Spada AR, Lafont, F, Lamark, T, Landry, J, Lane, Jd, Lapaquette, P, Laporte, Jf, László, L, Lavandero, S, Lavoie, Jn, Layfield, R, Lazo, Pa, Le, W, Le Cam, L, Ledbetter, Dj, Lee, Aj, Lee, Bw, Lee, Gm, Lee, J, Lee, Jh, Lee, M, Lee, Ms, Lee, Sh, Leeuwenburgh, C, Legembre, P, Legouis, R, Lehmann, M, Lei, Hy, Lei, Qy, Leib, Da, Leiro, J, Lemasters, Jj, Lemoine, A, Lesniak, Ms, Lev, D, Levenson, Vv, Levine, B, Levy, E, Li, F, Li, Jl, Li, L, Li, S, Li, W, Li, Xj, Li, Yb, Li, Yp, Liang, C, Liang, Q, Liao, Yf, Liberski, Pp, Lieberman, A, Lim, Hj, Lim, Kl, Lim, K, Lin, Cf, Lin, Fc, Lin, J, Lin, Jd, Lin, K, Lin, Ww, Lin, Wc, Lin, Yl, Linden, R, Lingor, P, Lippincott Schwartz, J, Lisanti, Mp, Liton, Pb, Liu, B, Liu, Cf, Liu, K, Liu, L, Liu, Qa, Liu, W, Liu, Yc, Liu, Y, Lockshin, Ra, Lok, Cn, Lonial, S, Loos, B, Lopez Berestein, G, López Otín, C, Lossi, L, Lotze, Mt, Lőw, P, Lu, B, Lu, Z, Luciano, F, Lukacs, Nw, Lund, Ah, Lynch Day MA, Ma, Y, Macian, F, Mackeigan, Jp, Macleod, Kf, Madeo, F, Maiuri, L, Maiuri, Mc, Malagoli, D, Malicdan, Mc, Malorni, W, Man, N, Mandelkow, Em, Manon, S, Manov, I, Mao, K, Mao, X, Mao, Z, Marambaud, P, Marazziti, D, Marcel, Yl, Marchbank, K, Marchetti, P, Marciniak, Sj, Marcondes, M, Mardi, M, Marfe, G, Mariño, G, Markaki, M, Marten, Mr, Martin, Sj, Martinand Mari, C, Martinet, W, Martinez Vicente, M, Masini, M, Matarrese, P, Matsuo, S, Matteoni, R, Mayer, A, Mazure, Nm, Mcconkey, Dj, Mcconnell, Mj, Mcdermott, C, Mcdonald, C, Mcinerney, Gm, Mckenna, Sl, Mclaughlin, B, Mclean, Pj, Mcmaster, Cr, Mcquibban, Ga, Meijer, Aj, Meisler, Mh, Meléndez, A, Melia, Tj, Melino, G, Mena, Ma, Menendez, Ja, Menna Barreto RF, Menon, Mb, Menzies, Fm, Mercer, Ca, Merighi, A, Merry, De, Meschini, S, Meyer, Cg, Meyer, Tf, Miao, Cy, Miao, Jy, Michels, Pa, Michiels, C, Mijaljica, D, Milojkovic, A, Minucci, S, Miracco, C, Miranti, Ck, Mitroulis, I, Miyazawa, K, Mizushima, N, Mograbi, B, Mohseni, S, Molero, X, Mollereau, B, Mollinedo, F, Momoi, T, Monastyrska, I, Monick, Mm, Monteiro, Mj, Moore, Mn, Mora, R, Moreau, K, Moreira, Pi, Moriyasu, Y, Moscat, J, Mostowy, S, Mottram, Jc, Motyl, T, Moussa, Ce, Müller, S, Muller, S, Münger, K, Münz, C, Murphy, Lo, Murphy, Me, Musarò, A, Mysorekar, I, Nagata, E, Nagata, K, Nahimana, A, Nair, U, Nakagawa, T, Nakahira, K, Nakano, H, Nakatogawa, H, Nanjundan, M, Naqvi, Ni, Narendra, Dp, Narita, M, Navarro, M, Nawrocki, St, Nazarko, Ty, Nemchenko, A, Netea, Mg, Neufeld, Tp, Ney, Pa, Nezis, Ip, Nguyen, Hp, Nie, D, Nishino, I, Nislow, C, Nixon, Ra, Noda, T, Noegel, Aa, Nogalska, A, Noguchi, S, Notterpek, L, Novak, I, Nozaki, T, Nukina, N, Nürnberger, T, Nyfeler, B, Obara, K, Oberley, Td, Oddo, S, Ogawa, M, Ohashi, T, Okamoto, K, Oleinick, Nl, Oliver, Fj, Olsen, Lj, Olsson, S, Opota, O, Osborne, Tf, Ostrander, Gk, Otsu, K, Ou, Jh, Ouimet, M, Overholtzer, M, Ozpolat, B, Paganetti, P, Pagnini, U, Pallet, N, Palmer, Ge, Palumbo, C, Pan, T, Panaretakis, T, Pandey, Ub, Papackova, Z, Papassideri, I, Paris, I, Park, J, Park, Ok, Parys, Jb, Parzych, Kr, Patschan, S, Patterson, C, Pattingre, S, Pawelek, Jm, Peng, J, Perlmutter, Dh, Perrotta, I, Perry, G, Pervaiz, S, Peter, M, Peters, Gj, Petersen, M, Petrovski, G, Phang, Jm, Piacentini, M, Pierre, P, Pierrefite Carle, V, Pierron, G, Pinkas Kramarski, R, Piras, A, Piri, N, Platanias, Lc, Pöggeler, S, Poirot, M, Poletti, A, Poüs, C, Pozuelo Rubio, M, Prætorius Ibba, M, Prasad, A, Prescott, M, Priault, M, Produit Zengaffinen, N, Progulske Fox, A, Proikas Cezanne, T, Przedborski, S, Przyklenk, K, Puertollano, R, Puyal, J, Qian, Sb, Qin, L, Qin, Zh, Quaggin, Se, Raben, N, Rabinowich, H, Rabkin, Sw, Rahman, I, Rami, A, Ramm, G, Randall, G, Randow, F, Rao, Va, Rathmell, Jc, Ravikumar, B, Ray, Sk, Reed, Bh, Reed, Jc, Reggiori, F, Régnier Vigouroux, A, Reichert, As, Reiners JJ Jr, Reiter, Rj, Ren, J, Revuelta, Jl, Rhodes, Cj, Ritis, K, Rizzo, E, Robbins, J, Roberge, M, Roca, H, Roccheri, Mc, Rocchi, S, Rodemann, Hp, Rodríguez de Córdoba, S, Rohrer, B, Roninson, Ib, Rosen, K, Rost Roszkowska MM, Rouis, M, Rouschop, Km, Rovetta, F, Rubin, Bp, Rubinsztein, Dc, Ruckdeschel, K, Rucker EB 3rd, Rudich, A, Rudolf, E, Ruiz Opazo, N, Russo, R, Rusten, Te, Ryan, Km, Ryter, Sw, Sabatini, Dm, Sadoshima, J, Saha, T, Saitoh, T, Sakagami, H, Sakai, Y, Salekdeh, Gh, Salomoni, P, Salvaterra, Pm, Salvesen, G, Salvioli, R, Sanchez, Am, Sánchez Alcázar JA, Sánchez Prieto, R, Sandri, M, Sankar, U, Sansanwal, P, Santambrogio, L, Saran, S, Sarkar, S, Sarwal, M, Sasakawa, C, Sasnauskiene, A, Sass, M, Sato, K, Sato, M, Schapira, Ah, Scharl, M, Schätzl, Hm, Scheper, W, Schiaffino, S, Schneider, C, Schneider, Me, Schneider Stock, R, Schoenlein, Pv, Schorderet, Df, Schüller, C, Schwartz, Gk, Scorrano, L, Sealy, L, Seglen, Po, Segura Aguilar, J, Seiliez, I, Seleverstov, O, Sell, C, Seo, Jb, Separovic, D, Setaluri, V, Setoguchi, T, Settembre, C, Shacka, Jj, Shanmugam, M, Shapiro, Im, Shaulian, E, Shaw, Rj, Shelhamer, Jh, Shen, Hm, Shen, Wc, Sheng, Zh, Shi, Y, Shibuya, K, Shidoji, Y, Shieh, Jj, Shih, Cm, Shimada, Y, Shimizu, S, Shintani, T, Shirihai, Os, Shore, Gc, Sibirny, Aa, Sidhu, Sb, Sikorska, B, Silva Zacarin EC, Simmons, A, Simon, Ak, Simon, Hu, Simone, C, Simonsen, A, Sinclair, Da, Singh, R, Sinha, D, Sinicrope, Fa, Sirko, A, Siu, Pm, Sivridis, E, Skop, V, Skulachev, Vp, Slack, Rs, Smaili, Ss, Smith, Dr, Soengas, Ms, Soldati, T, Song, X, Sood, Ak, Soong, Tw, Sotgia, F, Spector, Sa, Spies, Cd, Springer, W, Srinivasula, Sm, Stefanis, L, Steffan, Js, Stendel, R, Stenmark, H, Stephanou, A, Stern, St, Sternberg, C, Stork, B, Strålfors, P, Subauste, Cs, Sui, X, Sulzer, D, Sun, J, Sun, Sy, Sun, Zj, Sung, Jj, Suzuki, K, Suzuki, T, Swanson, Ms, Swanton, C, Sweeney, St, Sy, Lk, Szabadkai, G, Tabas, I, Taegtmeyer, H, Tafani, M, Takács Vellai, K, Takano, Y, Takegawa, K, Takemura, G, Takeshita, F, Talbot, Nj, Tan, Ks, Tanaka, K, Tang, D, Tanida, I, Tannous, Ba, Tavernarakis, N, Taylor, Gs, Taylor, Ga, Taylor, Jp, Terada, Ls, Terman, A, Tettamanti, G, Thevissen, K, Thompson, Cb, Thorburn, A, Thumm, M, Tian, F, Tian, Y, Tocchini Valentini, G, Tolkovsky, Am, Tomino, Y, Tönges, L, Tooze, Sa, Tournier, C, Tower, J, Towns, R, Trajkovic, V, Travassos, Lh, Tsai, Tf, Tschan, Mp, Tsubata, T, Tsung, A, Turk, B, Turner, Ls, Tyagi, Sc, Uchiyama, Y, Ueno, T, Umekawa, M, Umemiya, Shira, T., Aaltonen, B. A., Gonzalez, S., Amerio, D., Amidei, A., Anastassov, A., Annovi, J., Anto, G., Apollinari, J. A., Appel, T., Arisawa, A., Artikov, J., Asaadi, W., Ashmanska, B., Auerbach, A., Aurisano, F., Azfar, W., Badgett, T., Bae, A., Barbaro Galtieri, V. E., Barne, B. A., Barnett, P., Barria, P., Barto, M., Bauce, F., Bedeschi, S., Behari, G., Bellettini, J., Bellinger, D., Benjamin, A., Beretva, A., Bhatti, D., Bisello, I., Bizjak, K. R., Bland, B., Blumenfeld, A., Bocci, A., Bodek, D., Bortoletto, J., Boudreau, A., Boveia, L., Brigliadori, C., Bromberg, E., Brucken, J., Budagov, H. S., Budd, K., Burkett, G., Busetto, P., Bussey, A., Buzatu, A., Calamba, C., Calancha, S., Camarda, M., Campanelli, M., Campbell, F., Canelli, B., Carl, D., Carlsmith, R., Carosi, S., Carrillo, S., Carron, B., Casal, M., Casarsa, A., Castro, P., Catastini, D., Cauz, V., Cavaliere, M., Cavalli Sforza, A., Cerri, L., Cerrito, Y. C., Chen, M., Chertok, G., Chiarelli, G., Chlachidze, F., Chlebana, K., Cho, D., Chokheli, W. H., Chung, Y. S., Chung, M. A., Ciocci, A., Clark, C., Clarke, G., Compostella, M. E., Convery, J., Conway, M., Corbo, M., Cordelli, C. A., Cox, D. J., Cox, F., Crescioli, J., Cueva, R., Culbertson, D., Dagenhart, N., D'Ascenzo, M., Datta, P. D., Barbaro, M., Dell'Orso, L., Demortier, M., Deninno, F., Devoto, M., D'Errico, A. D., Canto, B. D., Ruzza, J. R., Dittmann, M., D'Onofrio, S., Donati, P., Dong, M., Dorigo, T., Dorigo, K., Ebina, A., Elagin, A., Eppig, R., Erbacher, S., Errede, N., Ershaidat, R., Eusebi, S., Farrington, M., Feindt, J. P., Fernandez, R., Field, G., Flanagan, R., Forrest, M. J., Frank, M., Franklin, J. C., Freeman, Y., Funakoshi, I., Furic, M., Gallinaro, J. E., Garcia, A. F., Garfinkel, P., Garosi, H., Gerberich, E., Gerchtein, S., Giagu, V., Giakoumopoulou, P., Giannetti, K., Gibson, C. M., Ginsburg, N., Giokari, P., Giromini, G., Giurgiu, V., Glagolev, D., Glenzinski, M., Gold, D., Goldin, N., Goldschmidt, A., Golossanov, G., Gomez, G., Gomez Ceballo, M., Goncharov, O., Gonzalez, I., Gorelov, A. T., Goshaw, K., Gouliano, L., Grillo, S., Grinstein, C., Grosso Pilcher, R. C., Group, J. G., Da, S. R., Hahn, E., Halkiadaki, A., Hamaguchi, J. Y., Han, F., Happacher, K., Hara, D., Hare, M., Hare, R. F., Harr, K., Hatakeyama, C., Hay, M., Heck, J., Heinrich, M., Herndon, S., Hewamanage, A., Hocker, W., Hopkin, D., Horn, S., Hou, R. E., Hughe, M., Hurwitz, U., Husemann, N., Hussain, M., Hussein, J., Huston, G., Introzzi, M., Iori, A., Ivanov, E., Jame, D., Jang, B., Jayatilaka, E. J., Jeon, S., Jindariani, M., Jone, K. K., Joo, S. Y., Jun, T. R., Junk, T., Kamon, P. E., Karchin, A., Kasmi, Y., Kato, W., Ketchum, J., Keung, V., Khotilovich, B., Kilminster, D. H., Kim, H. S., Kim, J. E., Kim, M. J., Kim, S. B., Kim, S. H., Kim, Y. K., Kim, Y. J., Kim, N., Kimura, M., Kirby, S., Klimenko, K., Knoepfel, K., Kondo, D. J., Kong, J., Konigsberg, A. V., Kotwal, M., Krep, J., Kroll, D., Krop, M., Kruse, V., Krutelyov, T., Kuhr, M., Kurata, S., Kwang, A. T., Laasanen, S., Lami, S., Lammel, M., Lancaster, R. L., Lander, K., Lannon, A., Lath, G., Latino, T., Lecompte, E., Lee, H. S., Lee, J. S., Lee, S. W., Lee, S., Leo, S., Leone, J. D., Lewi, A., Limosani, C. J., Lin, M., Lindgren, E., Lipele, A., Lister, D. O., Litvintsev, C., Liu, H., Liu, Q., Liu, T., Liu, S., Lockwitz, A., Loginov, D., Lucchesi, J., Lueck, P., Lujan, P., Luken, G., Lungu, J., Ly, R., Lysak, R., Madrak, K., Maeshima, P., Maestro, S., Malik, G., Manca, A., Manousakis Katsikaki, F., Margaroli, C., Marino, M., Martinez, P., Mastrandrea, K., Matera, M. E., Mattson, A., Mazzacane, P., Mazzanti, K. S., Mcfarland, P., Mcintyre, R., Mcnulty, A., Mehta, P., Mehtala, C., Mesropian, T., Miao, D., Mietlicki, A., Mitra, H., Miyake, S., Moed, N., Moggi, M. N., Mondragon, C. S., Moon, R., Moore, Morello, MICHAEL JOSEPH, J., Morlock, P. M., Fernandez, A., Mukherjee, T., Muller, P., Murat, M., Mussini, J., Nachtman, Y., Nagai, J., Naganoma, I., Nakano, A., Napier, J., Nett, C., Neu, M. S., Neubauer, J., Nielsen, L., Nodulman, S. Y., Noh, O., Norniella, L., Oake, S. H., Oh, Y. D., Oh, I., Oksuzian, T., Okusawa, R., Orava, L., Ortolan, S. P., Griso, C., Pagliarone, E., Palencia, V., Papadimitriou, A. A., Paramonov, J., Patrick, G., Pauletta, M., Paulini, C., Pau, D. E., Pellett, A., Penzo, T. J., Phillip, G., Piacentino, E., Pianori, J., Pilot, K., Pitt, C., Plager, L., Pondrom, S., Poprocki, K., Potamiano, F., Prokoshin, A., Pranko, F., Ptoho, G., Punzi, A., Rahaman, V., Ramakrishnan, N., Ranjan, I., Redondo, P., Renton, M., Rescigno, T., Riddick, F., Rimondi, L., Ristori, A., Robson, T., Rodrigo, T., Rodriguez, E., Roger, S., Rolli, R., Roser, F., Ruffini, A., Ruiz, J., Ru, V., Rusu, A., Safonov, W. 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Aaltonen, B. Álvarez González, S. Amerio, D. Amidei, A. Anastassov, A. Annovi, J. Anto, G. Apollinari, J. Appel, T. Arisawa, A. Artikov, J. Asaadi, W. Ashmanska, B. Auerbach, A. Aurisano, F. Azfar, W. Badgett, T. Bae, A. Barbaro-Galtieri, V. Barne, B. Barnett, P. Barria, P. Barto, M. Bauce, F. Bedeschi, S. Behari, G. Bellettini, J. Bellinger, D. Benjamin, A. Beretva, A. Bhatti, D. Bisello, I. Bizjak, K. Bland, B. Blumenfeld, A. Bocci, A. Bodek, D. Bortoletto, J. Boudreau, A. Boveia, L. Brigliadori, C. Bromberg, E. Brucken, J. Budagov, H. Budd, K. Burkett, G. Busetto, P. Bussey, A. Buzatu, A. Calamba, C. Calancha, S. Camarda, M. Campanelli, M. Campbell, F. Canelli, B. Carl, D. Carlsmith, R. Carosi, S. Carrillo, S. Carron, B. Casal, M. Casarsa, A. Castro, P. Catastini, D. Cauz, V. Cavaliere, M. Cavalli-Sforza, A. Cerri, L. Cerrito, Y. Chen, M. Chertok, G. Chiarelli, G. Chlachidze, F. Chlebana, K. Cho, D. Chokheli, W. Chung, Y. Chung, M. Ciocci, A. Clark, C. Clarke, G. Compostella, M. Convery, J. Conway, M. Corbo, M. Cordelli, C. Cox, D. Cox, F. Crescioli, J. Cueva, R. Culbertson, D. Dagenhart, N. d’Ascenzo, M. Datta, P. de Barbaro, M. Dell’Orso, L. Demortier, M. Deninno, F. Devoto, M. d’Errico, A. Di Canto, B. Di Ruzza, J. Dittmann, M. D’Onofrio, S. Donati, P. Dong, M. Dorigo, T. Dorigo, K. Ebina, A. Elagin, A. Eppig, R. Erbacher, S. Errede, N. Ershaidat, R. Eusebi, S. Farrington, M. Feindt, J. Fernandez, R. Field, G. Flanagan, R. Forrest, M. Frank, M. Franklin, J. Freeman, Y. Funakoshi, I. Furic, M. Gallinaro, J. Garcia, A. Garfinkel, P. Garosi, H. Gerberich, E. Gerchtein, S. Giagu, V. Giakoumopoulou, P. Giannetti, K. Gibson, C. Ginsburg, N. Giokari, P. Giromini, G. Giurgiu, V. Glagolev, D. Glenzinski, M. Gold, D. Goldin, N. Goldschmidt, A. Golossanov, G. Gomez, G. Gomez-Ceballo, M. Goncharov, O. González, I. Gorelov, A. Goshaw, K. Gouliano, L. Grillo, S. Grinstein, C. Grosso-Pilcher, R. Group, J. Guimaraes da Costa, S. Hahn, E. Halkiadaki, A. Hamaguchi, J. Han, F. Happacher, K. Hara, D. Hare, M. Hare, R. Harr, K. Hatakeyama, C. Hay, M. Heck, J. Heinrich, M. Herndon, S. Hewamanage, A. Hocker, W. Hopkin, D. Horn, S. Hou, R. Hughe, M. Hurwitz, U. Husemann, N. Hussain, M. Hussein, J. Huston, G. Introzzi, M. Iori, A. Ivanov, E. Jame, D. Jang, B. Jayatilaka, E. Jeon, S. Jindariani, M. Jone, K. Joo, S. Jun, T. Junk, T. Kamon, P. Karchin, A. Kasmi, Y. Kato, W. Ketchum, J. Keung, V. Khotilovich, B. Kilminster, D. Kim, H. Kim, J. Kim, M. Kim, S. Kim, Y. Kim, N. Kimura, M. Kirby, S. Klimenko, K. Knoepfel, K. Kondo, D. Kong, J. Konigsberg, A. Kotwal, M. Krep, J. Kroll, D. Krop, M. Kruse, V. Krutelyov, T. Kuhr, M. Kurata, S. Kwang, A. Laasanen, S. Lami, S. Lammel, M. Lancaster, R. Lander, K. Lannon, A. Lath, G. Latino, T. LeCompte, E. Lee, H. Lee, J. Lee, S. Lee, S. Leo, S. Leone, J. Lewi, A. Limosani, C.-J. Lin, M. Lindgren, E. Lipele, A. Lister, D. Litvintsev, C. Liu, H. Liu, Q. Liu, T. Liu, S. Lockwitz, A. Loginov, D. Lucchesi, J. Lueck, P. Lujan, P. Luken, G. Lungu, J. Ly, R. Lysak, R. Madrak, K. Maeshima, P. Maestro, S. Malik, G. Manca, A. Manousakis-Katsikaki, F. Margaroli, C. Marino, M. Martínez, P. Mastrandrea, K. Matera, M. Mattson, A. Mazzacane, P. Mazzanti, K. McFarland, P. McIntyre, R. McNulty, A. Mehta, P. Mehtala, C. Mesropian, T. Miao, D. Mietlicki, A. Mitra, H. Miyake, S. Moed, N. Moggi, M. Mondragon, C. Moon, R. Moore, M. Morello, J. Morlock, P. Movilla Fernandez, A. Mukherjee, Th. Muller, P. Murat, M. Mussini, J. Nachtman, Y. Nagai, J. Naganoma, I. Nakano, A. Napier, J. Nett, C. Neu, M. Neubauer, J. Nielsen, L. Nodulman, S. Noh, O. Norniella, L. Oake, S. Oh, Y. Oh, I. Oksuzian, T. Okusawa, R. Orava, L. Ortolan, S. Pagan Griso, C. Pagliarone, E. Palencia, V. Papadimitriou, A. Paramonov, J. Patrick, G. Pauletta, M. Paulini, C. Pau, D. Pellett, A. Penzo, T. Phillip, G. Piacentino, E. Pianori, J. Pilot, K. Pitt, C. Plager, L. Pondrom, S. Poprocki, K. Potamiano, F. Prokoshin, A. Pranko, F. Ptoho, G. Punzi, A. Rahaman, V. Ramakrishnan, N. Ranjan, I. Redondo, P. Renton, M. Rescigno, T. Riddick, F. Rimondi, L. Ristori, A. Robson, T. Rodrigo, T. Rodriguez, E. Roger, S. Rolli, R. Roser, F. Ruffini, A. Ruiz, J. Ru, V. Rusu, A. Safonov, W. Sakumoto, Y. Sakurai, L. Santi, K. Sato, V. Saveliev, A. Savoy-Navarro, P. Schlabach, A. Schmidt, E. Schmidt, T. Schwarz, L. Scodellaro, A. Scribano, F. Scuri, S. Seidel, Y. Seiya, A. Semenov, F. Sforza, S. Shalhout, T. Shear, P. Shepard, M. Shimojima, M. Shochet, I. Shreyber-Tecker, A. Simonenko, P. Sinervo, K. Sliwa, J. Smith, F. Snider, A. Soha, V. Sorin, H. Song, P. Squillacioti, M. Stancari, R. St. Deni, B. Stelzer, O. Stelzer-Chilton, D. Stentz, J. Strologa, G. Strycker, Y. Sudo, A. Sukhanov, I. Suslov, K. Takemasa, Y. Takeuchi, J. Tang, M. Tecchio, P. Teng, J. Thom, J. Thome, G. Thompson, E. Thomson, D. Toback, S. Tokar, K. Tollefson, T. Tomura, D. Tonelli, S. Torre, D. Torretta, P. Totaro, M. Trovato, F. Ukegawa, S. Uozumi, A. Varganov, F. Vázquez, G. Velev, C. Vellidi, M. Vidal, I. Vila, R. Vilar, J. Vizán, M. Vogel, G. Volpi, P. Wagner, R. Wagner, T. Wakisaka, R. Wallny, S. Wang, A. Warburton, D. Water, W. Wester, D. Whiteson, A. Wicklund, E. Wicklund, S. Wilbur, F. Wick, H. William, J. Wilson, P. Wilson, B. Winer, P. Wittich, S. Wolber, H. Wolfe, T. Wright, X. Wu, Z. Wu, K. Yamamoto, D. Yamato, T. Yang, U. Yang, Y. Yang, W.-M. Yao, G. Yeh, K. Yi, J. Yoh, K. Yorita, T. Yoshida, G. Yu, I. Yu, S. Yu, J. Yun, A. Zanetti, Y. Zeng, C. Zhou, S. Zucchelli, and Universidad de Cantabria

Subjects
FERMILAB TEVATRON COLLIDER, Particle physics, CP-violating asymmetries, Meson, B physic, General Physics and Astronomy, FOS: Physical sciences, B physics, Angle distribution, Branching ratio, CDF experiments, CP violations, CP-violating asymmetries, Data sample, Fermilab Tevatron collider, Integrated luminosity, Longitudinal polarization, Vector meson, Longitudinal polarization, 7. Clean energy, 01 natural sciences, High Energy Physics - Experiment, Vector meson, Physics and Astronomy (all), High Energy Physics - Experiment (hep-ex), High Energy Physics - Phenomenology (hep-ph), Mixing (mathematics), Strange b mesons, Phase (matter), 0103 physical sciences, STRANGE QUARK, mixing, Bottom-Strange Meson Mixing Phase, proton antiproton collisions, 010306 general physics, TEVATRON, Nuclear Experiment, BOTTOM QUARK, Physics, Integrated luminosity, 010308 nuclear & particles physics, Branching ratio, High Energy Physics - Phenomenology, CDF experiments, CP violations, Full data, Content (measure theory), Angle distribution, CDF, Production (computer science), High Energy Physics::Experiment, Data sample
Abstract

We report a measurement of the bottom-strange meson mixing phase βs using the time evolution of Bs0→J/ψ(→μ+μ-)ϕ(→K+K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at s=1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of βs and the Bs0 decay-width difference ΔΓs and measure βs∈[-π/2,-1.51]∪[-0.06,0.30]∪[1.26,π/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of βs, we also determine ΔΓs=0.068±0.026(stat)±0.009(syst) ps-1 and the mean Bs0 lifetime τs=1.528±0.019(stat)±0.009(syst) ps, which are consistent and competitive with determinations by other experiments., This work was supported by the U.S. Department of Energy and National Science Foundation; the Italian Istituto Nazionale di Fisica Nucleare; the Ministry of Education, Culture, Sports, Science and Technology of Japan; the Natural Sciences and Engineering Research Council of Canada; the National Science Council of the Republic of China; the Swiss National Science Foundation; the A. P. Sloan Foundation; the Bundesministerium für Bildung und Forschung, Germany; the Korean World Class University Program, the National Research Foundation of Korea; the Science and Technology Facilities Council and the Royal Society, UK; the Russian Foundation for Basic Research; the Ministerio de Ciencia e Innovación, and Programa Consolider-Ingenio 2010, Spain; the Slovak R&D Agency; the Academy of Finland; and the Australian Research Council (ARC).

Published
2012

28. Neuromelanins in brain aging and Parkinson's disease

Author

Zecca L., Zhang W., Jackson-Lewis V., Przedborski S., Hong J.S., Sulzer D., Bellei C., Casella L., Turro N.J., Eisner M., Crippa P.R., Ito S., Wakamatsu K., Simon J.D., and Zucca F.A.

Published
2011

35. Lanosterol induces mitochondrial uncoupling and protects dopaminergic neurons from cell death in a model for Parkinson's disease

Author

Jenner, Andrew M., Shui, Guanghou, Wenk, M. R., Lim, L., Jackson-Lewis, V., Przedborski, S., Kesavapany, S., Goh, A. X. H., Fivaz, M., Wong, L. C., Jenner, Andrew M., Shui, Guanghou, Wenk, M. R., Lim, L., Jackson-Lewis, V., Przedborski, S., Kesavapany, S., Goh, A. X. H., Fivaz, M., and Wong, L. C.

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder marked by the selective degeneration of dopaminergic neurons in the nigrostriatal pathway. Several lines of evidence indicate that mitochondrial dysfunction contributes to its etiology. Other studies have suggested that alterations in sterol homeostasis correlate with increased risk for PD. Whether these observations are functionally related is, however, unknown. In this study, we used a toxin-induced mouse model of PD and measured levels of nine sterol intermediates. We found that lanosterol is significantly (~50%) and specifically reduced in the nigrostriatal regions of 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine-treated mice, indicative of altered lanosterol metabolism during PD pathogenesis. Remarkably, exogenous addition of lanosterol rescued dopaminergic neurons from 1-methyl-4-phenylpyridinium (MPP+)-induced cell death in culture. Furthermore, we observed a marked redistribution of lanosterol synthase from the endoplasmic reticulum to mitochondria in dopaminergic neurons exposed to MPP, suggesting that lanosterol might exert its survival effect by regulating mitochondrial function. Consistent with this model, we find that lanosterol induces mild depolarization of mitochondria and promotes autophagy. Collectively, our results highlight a novel sterol-based neuroprotective mechanism with direct relevance to PD. © 2012 Macmillan Publishers Limited All rights reserved.

Published
2012

36. Guidelines for the use and interpretation of assays for monitoring autophagy.

Author

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Zuckerbraun, B., and Viscomi M. T. (ORCID:0000-0002-9096-4967)

Abstract

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused o

Published
2012

37. Lanosterol induces mitochondrial uncoupling and protects dopaminergic neurons from cell death in a model for Parkinson's disease.

Author

Lim, L, Jackson-Lewis, V, Wong, L C, Shui, G H, Goh, A X H, Kesavapany, S, Jenner, A M, Fivaz, M, Przedborski, S, Wenk, M R, Lim, L, Jackson-Lewis, V, Wong, L C, Shui, G H, Goh, A X H, Kesavapany, S, Jenner, A M, Fivaz, M, Przedborski, S, and Wenk, M R

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder marked by the selective degeneration of dopaminergic neurons in the nigrostriatal pathway. Several lines of evidence indicate that mitochondrial dysfunction contributes to its etiology. Other studies have suggested that alterations in sterol homeostasis correlate with increased risk for PD. Whether these observations are functionally related is, however, unknown. In this study, we used a toxin-induced mouse model of PD and measured levels of nine sterol intermediates. We found that lanosterol is significantly (∼50%) and specifically reduced in the nigrostriatal regions of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mice, indicative of altered lanosterol metabolism during PD pathogenesis. Remarkably, exogenous addition of lanosterol rescued dopaminergic neurons from 1-methyl-4-phenylpyridinium (MPP+)-induced cell death in culture. Furthermore, we observed a marked redistribution of lanosterol synthase from the endoplasmic reticulum to mitochondria in dopaminergic neurons exposed to MPP+, suggesting that lanosterol might exert its survival effect by regulating mitochondrial function. Consistent with this model, we find that lanosterol induces mild depolarization of mitochondria and promotes autophagy. Collectively, our results highlight a novel sterol-based neuroprotective mechanism with direct relevance to PD.

Published
2012

44. Cyclin-dependent kinase 5 is a mediator of dopaminergic neuron loss in a mouse model of Parkinson's disease

Author

Smith, P. (Patrice D.), Crocker, S.J. (Stephen J.), Jackson-Lewis, V. (Vernice), Jordan-Sciutto, K.L. (Kelly L.), Hayley, S. (Shawn), Mount, M.P. (Matthew P.), O'Hare, M.J. (Michael J.), Callaghan, S. (Steven), Slack, R.S. (Ruth S.), Przedborski, S. (Serge), Anisman, H. (Hymie), Park, D.S. (David S.), Smith, P. (Patrice D.), Crocker, S.J. (Stephen J.), Jackson-Lewis, V. (Vernice), Jordan-Sciutto, K.L. (Kelly L.), Hayley, S. (Shawn), Mount, M.P. (Matthew P.), O'Hare, M.J. (Michael J.), Callaghan, S. (Steven), Slack, R.S. (Ruth S.), Przedborski, S. (Serge), Anisman, H. (Hymie), and Park, D.S. (David S.)

Abstract

Recent evidence indicates that cyclin-dependent kinases (CDKs, cdks) may be inappropriately activated in several neurodegenerative conditions. Here, we report that cdk5 expression and activity are elevated after administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin that damages the nigrostriatal dopaminergic pathway. Supporting the pathogenic significance of the cdk5 alterations are the findings that the general cdk inhibitor, flavopiridol, or expression of dominant-negative cdk5, and to a lesser extent dominant-negative cdk2, attenuates the loss of dopaminergic neurons caused by MPTP. In addition, CDK inhibition strategies attenuate MPTP-induced hypolocomotion and markers of striatal function independent of striatal dopamine. We propose that cdk5 is a key regulator in the degeneration of dopaminerg

Published
2003
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49. [Current therapeutic approach in Parkinson disease]

Author

Przedborski S and Marc Levivier

Subjects
Antiparkinson Agents, Levodopa, Apomorphine, Fetal Tissue Transplantation, Mesencephalon, Selegiline, Humans, Vitamin E, Parkinson Disease, Bromocriptine
Abstract

Parkinson's disease is a neurodegenerative disorder characterized mainly by a loss of the dopaminergic neurons of the nigrostriatal pathway. The symptomatic treatment, which consists of the supply of the deficient neurotransmitter dopamine, does not, however, prevent the progression of the disease and is frequently associated with major motor and psychiatric side effects. Recent basic and clinical investigations have led to the development of new therapeutical strategies for Parkinson's disease. The authors review and describe these new approaches which include: [1] treatments aimed at slowing down the progression of the disease, [2] treatments aimed at decreasing the motor side effects and [3] the use of intracerebral transplantations.

Published
1992

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