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53. Progressive supranuclear palsy: loss of choline-acetyltransferase-like immunoreactive neurons in the pontine reticular formation

Author

Malessa, S., Hirsch, E.C., Cervera, P., Javoy-Agid, F., Duyckaerts, C., Hauw, J.J., and Agid, Y.

Subjects
Progressive supranuclear palsy -- Physiological aspects, Eye -- Movements, Cholinergic mechanisms -- Physiological aspects, Health, Psychology and mental health
Abstract

Progressive supranuclear palsy (PSP) is a degenerative brain disorder in which the patient develops many neurological symptoms including dementia and unstable posture. The term 'supranuclear palsy' refers to the fact that the paralysis results from lesions above the level of brainstem nerve nuclei. Pathological examination reveals damage in many parts of the brain. Abnormal findings such as neurofibrillary tangles, loss of brain cells, and gliosis are found in the globus pallidus, subthalamic nucleus, and other parts of the brain. Abnormalities of eye movements are also part of the syndrome of PSP, and some impairments get worse as the PSP progresses. Since much of the control of eye movements is centered in a part of the brain called the pontine reticular formation, this region was singled out for a detailed anatomical study. The brains of three patients with PSP and four control patients were examined. The brain regions were stained using immunocytochemical techniques, and antibodies that are specific for the enzyme choline acetyltransferase (ChAT). Two nuclei, or clusters of nerve cell bodies, were identified that were abnormal when compared with the control tissues. The nucleus papilloformis and the nucleus pontis centralis caudalis both stained with the ChAT antibodies. However, there were 46 and 60 percent fewer neurons than normal in the nucleus papilloformis and the nucleus pontis centralis caudalis, respectively. Since ChAT is regarded as a reliable indicator of nerve systems using the neurotransmitter substance acetylcholine, these results would indicate that cholinergic systems that serve eye movements are profoundly affected by the PSP disease process. However, it is not clear from the present study whether all nerve cells in this region are affected by PSP or whether the cholinergic systems are preferentially singled out for damage. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

54. Mesencephalic cholinergic nuclei in progressive supranuclear palsy

Author

Juncos, J.L., Hirsch, E.C., Malessa, S., Duyckaerts, C., Hersh, L.B., and Agid, Y.

Subjects
Progressive supranuclear palsy -- Physiological aspects, Mesencephalon, Acetylcholine -- Physiological aspects, Transferases -- Physiological aspects, Health, Psychology and mental health
Abstract

The phrase 'supranuclear palsy' refers to a spastic weakness of muscles innervated by the cranial nerves. The term 'supranuclear' implies that the lesion responsible for the symptoms is above the level of the cranial nerve nuclei. Progressive supranuclear palsy (PSP) is a completely distinct disease, in which the symptoms of supranuclear palsy (also called pseudobulbar palsy) are combined with postural instability, dementia, dystonia (abnormal muscle tone) and impaired voluntary eye movements. As its name implies, progressive supranuclear palsy is a progressive neurodegenerative disease. Pathologic examination of the brains of victims of PSP reveals neurofibrillary tangles, granulovacuolar degeneration, and gliosis. Some investigators, but not all, have found a deficit in brain systems within the basal ganglia that use the neurotransmitter acetylcholine. A similar loss of cholinergic neurons has been reported in the brainstem. In this study, the authors performed a careful histologic examination of several regions in the mesencephalon of the brains of three patients who died of PSP as well as the brains of four control subjects. Antibodies were used to specifically stain the enzyme choline acetyltransferase, which is found in neurons that manufacture acetylcholine. Antibodies to this enzyme are superior to those of the enzyme acetylcholinesterase for marking the location of cholinergic neurons within microscopic brain sections. Upon examining the brains, the researchers found that the numbers of cholinergic neurons were significantly depleted in some brain regions. A significant decrease in the number of choline acetyltransferase-containing neurons was found in the nucleus of Edinger-Westphal, the rostral interstitial nucleus of the medial longitudinal fasciculus, and the interstitial nucleus of Cajal. There were also signs of cell loss in the deep layers of the superior colliculus. There were no differences between the control and the PSP brains in the nuclei of nerves III and IV, in the mesencephalic reticular formation, or the parabigeminal nucleus. The results confirm a cholinergic deficit in PSP, and also indicate that the deficit is found in some specific brain regions, but not in all. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

56. Age-induced cognitive disturbances in Parkinson's disease

Author

Dubois, B., Pillon, B., Sternic, N., Lhermitte, F., and Agid, Y.

Subjects
Parkinsonism -- Development and progression, Parkinsonism -- Demographic aspects, Cognition disorders -- Development and progression, Health, Psychology and mental health
Abstract

Parkinson's disease is most noted for tremor, rigidity, and slow movement. Patients with Parkinson's disease often develop memory deficits and difficulties with reasoning and other intellectual functions. However, these complications are not evenly distributed among all Parkinson's patients; they tend to be more common among patients who developed Parkinson's disease later in life. A study was undertaken to compare the intellectual disturbances in patients who developed Parkinson's disease at a younger age with those who developed the disorder later in life. The cases of 11 patients who developed Parkinson's disease before the age of 45 were compared with 11 patients who developed the disorder after 65. Each group of 11 was also compared with 11 healthy control subjects matched for age. Psychological testing revealed some intellectual deficits in the younger subjects, but these deficits were mild and the patients could largely compensate for them in their daily activities. Indeed, only the more complex of the psychological tests revealed the difficulty. The same was not true of the older patients, however. Testing of the older patients revealed more total intellectual deterioration. In addition to moderate memory problems, there were intellectual deficits that were of the sort associated with abnormal function of the frontal lobes of the brain. However, the language functions of these older patients were well preserved, a pattern common among patients with Parkinson's disease. The increased deficit of the older patients cannot be attributed entirely to their age, since similar deficits were not seen in the age-matched controls. Therefore, it seems that in younger patients with Parkinson's disease the deterioration is largely confined to movement. In older patients, however, the progression of movement disorders is soon followed by progressive deterioration of intellectual function as well. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

67. Causal relation between [alpha]-synuclein locus duplication as a cause of familial Parkinson's disease

Author

IbaA[+ or -]ez, P., Bonnet, A-M, Debarges, B., Lohmann, E., Tison, F., Pollak, P., Agid, Y., Durr, A., and Brice, A.

Subjects
Nerve proteins -- Physiological aspects, Nerve proteins -- Genetic aspects, Nerve proteins -- Research, Parkinson's disease -- Causes of, Parkinson's disease -- Genetic aspects, Parkinson's disease -- Research, Polymerase chain reaction -- Usage, Polymerase chain reaction -- Research
Published
2004

76. The parkin gene and its phenotype

Author

Bonifati, V., De Michele, G., Lücking, C. B., Dürr, A., Fabrizio, E., Ambrosio, G., Vanacore, N., De Mari, M., Marconi, R., Capus, L., Breteler, M. M. B., Gasser, T., Oostra, B., Wood, N., Agid, Y., Filla, A., Meco, G., Brice, A., and for the Italian PD Genetics Study Group, French PD Genetics Study Groupand the European Consortium on Genetic Susceptibility in Parkinson's Disease

Published
2001
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84. Neurochemical Investigations into the Human Area Postrema

Author

Schwartz, J.-C., Agid, Y., Bouthenet, M.-L., Javoy-Agid, F., Llorens-Cortes, C., Martres, M.-P., Pollard, H., Sales, N., Taquet, H., Joynt, R. J., editor, Weindl, A., editor, Davis, Christopher J., editor, Lake-Bakaar, Gerry V., editor, and Grahame-Smith, David G., editor

Published
1986
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88. Phenotype, genotype, and worldwide genetic penetrance of LRRK2-associated Parkinson's disease: a case-control study

Author

Healy, Daniel G., Mario, Falchi, O'Sullivan, Sean S., Bonifati, Vincenzo, Alexandra, Durr, Susan, Bressman, Alexis, Brice, Jan, Aasly, Zabetian, Cyrus P., Stefano, Goldwurm, Ferreira, Joaquim J., Eduardo, Tolosa, Kay, Denise M., Christine, Klein, Williams, David R., Connie, Marras, Lang, Anthony E., Wszolek, Zbigniew K., Jose, Berciano, Schapira, Anthony H. V., Timothy, Lynch, Bhatia, Kailash P., Thomas, Gasser, Lees, Andrew J., Wood, Nicholas W., International Lrrk Consortium, Collaborators, Tazir, M., Ysmail Dahlouk, F., Belarbi, S., Hecham, N., Barbosa, E., Chien, H. F., Rieder, C. R., Jardim, L. B., Rogaeva, E., Lesage, S., Lohmann, E., Vidailhet, M., Bonnet, A. M., Agid, Y., Pollak, P., Tison, F., Durif, F., Broussolle, E., Berg, D., Hagenah, J., Gosal, D., Gibson, M., Vanacore, Nicola, Berardelli, Alfredo, Fabbrini, Giovanni, Fabrizio, E., Meco, Giuseppe, Stocchi, F., Dalla Libera, A., De Mari, M., Lamberti, P., Cossu, G., Pezzoli, G., Zini, M., Tesei, S., Zecchinelli, A., Sironi, F., Antonini, A., Mariani, C., Sacilotto, G., Meucci, N., Canesi, M., Di Fonzo, A., Oostra, B., Correia Guedes, L., Rosa, Mm, Coelho, M., Sampaio, C., Gaig, C., C. S., Lu, Wu Chou, Y. H., Quinn, N. P., Abou Sleiman, P. M., Muqit, M. M., Khan, N. L., Gandhi, S., Vaughan, J., Payami, H., Nutt, J. J., Factor, S. A., Higgins, D. S., Farrer, M. J., Hulihan, M., Brown, L., Mata, I. F., Samii, A., Yearout, D., Griffith, A., Leis, B. C., Roberts, J. W., Clinical Genetics, Department of Clinical Neurosciences, University College of London [London] (UCL)-Institute of Neurology, Genomic Medicine, Imperial College London-Kings College, Reta Lila Weston Institute for Neurological Studies, Queen Mary University of London (QMUL), Department of Clinical Genetics (DCG), Erasmus University Medical Centre, CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière (CRICM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Department of Neurology, Beth Israel Medical Centre- Albert Einstein College of Medicine [New York], St. Olav's Hospital, University of Washington [Seattle], Geriatric Research Education and Clinical Center, VA Puget Sound Health Care System, Parkinson Institute, Istituti Clinici di Perfezionamento, Neurological Clinic Research Unit, Institute of Molecular Medicine-Lisbon School of Medicine, Neurology Service, Institut Clinic Maltias del Sistema Nervios-Hospital Clinic Universitari-University of Barcelona, Division of Genetic Disorders, New York State Department of Health [Albany], University of Luebeck, Faculty of Medicine (Neurosciences), Monash University [Clayton], University of Toronto, Mayo Clinic Jacksonville, Service of Neurology, Centro de Investigacion Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Instituto de Salud Carlos III [Madrid] (ISC)-Instituto de Salud Carlos III [Madrid] (ISC), Mater Misericordiae University Hospital (The Mater Hospital), Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Department of Neurodegenerative Diseases, Eberhard Karls Universität Tübingen = Eberhard Karls University of Tuebingen-Hertie-Institut for Clinical Brain Research, Department of Molecular Pathogenesis, UK Medical Research Council, UK Parkinson's Disease Society, UK Brain Research Trust, Internationaal Parkinson Fonds, Volkswagen Foundation, National Institutes of Health: National Institute of Neurological Disorders and Stroke and National Institute of Aging, Udall Parkinson's Disease Centre of Excellence, Pacific Alzheimer Research Foundation Centre, Italian Telethon Foundation, Fondazione Grigioni per il Morbo di Parkinson, Michael J Fox Foundation for Parkinson's Research, Safra Global Genetics Consortium, US Department of Veterans Affairs, French Agence Nationale de la Recherche., ANR-05-NEUR-0019,LRRK2 in PD,Pathologie moléculaire et modèles murins du gène LRRK2, impliqué dans la maladie de Parkinson(2005), Service de Génétique Cytogénétique et Embryologie [CHU Pitié-Salpêtrière], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Pitié-Salpêtrière [APHP], Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC), Beth Israel Medical Centre- Albert Einstein College of Medicine, CIBER de Enfermedades Neurodegenerativas (CIBERNED), Mater Misericordiae University Hospital, Eberhard Karls Universität Tübingen-Hertie-Institut for Clinical Brain Research, ANR-05-NEURO-019,ANR-05-NEURO-019, and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)

Subjects
Gerontology, Male, Risk, Pediatrics, medicine.medical_specialty, Parkinson's disease, Genotype, International Cooperation, DNA Mutational Analysis, Glycine, Clinical Neurology, Penetrance, Disease, Protein Serine-Threonine Kinases, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Severity of Illness Index, 03 medical and health sciences, 0302 clinical medicine, medicine, Serine, Humans, Genetic Predisposition to Disease, Genetic Testing, Age of Onset, 030304 developmental biology, Genetic testing, Family Health, 0303 health sciences, medicine.diagnostic_test, business.industry, Case-control study, Age Factors, Parkinson Disease, medicine.disease, LRRK2, 3. Good health, nervous system diseases, Dyskinesia, Case-Control Studies, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Female, Neurology (clinical), genetics, parkinson, Age of onset, medicine.symptom, business, 030217 neurology & neurosurgery
Abstract

Summary Background Mutations in LRRK2 , the gene that encodes leucine-rich repeat kinase 2, are a cause of Parkinson's disease (PD). The International LRRK2 Consortium was established to answer three key clinical questions: can LRRK2 -associated PD be distinguished from idiopathic PD; which mutations in LRRK2 are pathogenic; and what is the age-specific cumulative risk of PD for individuals who inherit or are at risk of inheriting a deleterious mutation in LRRK2 ? Methods Researchers from 21 centres across the world collaborated on this study. The frequency of the common LRRK2 Gly2019Ser mutation was estimated on the basis of data from 24 populations worldwide, and the penetrance of the mutation was defined in 1045 people with mutations in LRRK2 from 133 families. The LRRK2 phenotype was defined on the basis of 59 motor and non-motor symptoms in 356 patients with LRRK2 -associated PD and compared with the symptoms of 543 patients with pathologically proven idiopathic PD. Findings Six mutations met the consortium's criteria for being proven pathogenic. The frequency of the common LRRK2 Gly2019Ser mutation was 1% of patients with sporadic PD and 4% of patients with hereditary PD; the frequency was highest in the middle east and higher in southern Europe than in northern Europe. The risk of PD for a person who inherits the LRRK2 Gly2019Ser mutation was 28% at age 59 years, 51% at 69 years, and 74% at 79 years. The motor symptoms (eg, disease severity, rate of progression, occurrence of falls, and dyskinesia) and non-motor symptoms (eg, cognition and olfaction) of LRRK2 -associated PD were more benign than those of idiopathic PD. Interpretation Mutations in LRRK2 are a clinically relevant cause of PD that merit testing in patients with hereditary PD and in subgroups of patients with PD. However, this knowledge should be applied with caution in the diagnosis and counselling of patients. Funding UK Medical Research Council; UK Parkinson's Disease Society; UK Brain Research Trust; Internationaal Parkinson Fonds; Volkswagen Foundation; National Institutes of Health: National Institute of Neurological Disorders and Stroke and National Institute of Aging; Udall Parkinson's Disease Centre of Excellence; Pacific Alzheimer Research Foundation Centre; Italian Telethon Foundation; Fondazione Grigioni per il Morbo di Parkinson; Michael J Fox Foundation for Parkinson's Research; Safra Global Genetics Consortium; US Department of Veterans Affairs; French Agence Nationale de la Recherche.

Published
2008
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95. Parkin mutations are frequent in patients with isolated early-onset parkinsonism

Author

Periquet, M, Latouche, M, Lohmann, E, Rawal, N, De Michele, G, Ricard, S, Teive, H, Fraix, V, Vidailhet, M, Nicholl, D, Barone, Paolo, Wood, Nw, Raskin, S, Deleuze, Jf, Agid, Y, Dürr, A, Brice, A, French Parkinson's Disease Genetics Study Group, European Consortium on Genetic Susceptibility in Parkinson's Disease, Periquet, M, Latouche, M, Lohmann, E, Rawal, N, DE MICHELE, Giuseppe, Ricard, S, Teive, H, Fraix, V, Vidailhet, M, Nicholl, D, Barone, P, Wood, Nw, Raskin, S, Deleuze, Jf, Agid, Y, Durr, A, Brice, A, FRENCH PARKINSON'S DISEASE GENETICS STUDY, Group, and EUROPEAN CONSORTIUM ON GENETIC SUSCEPTIBILITY IN PARKINSON'S, Disease

Published
2003

96. Screening for DJ-1 mutations in early onset autosomal recessive parkinsonism

Author

IBANEZ P, BONIFATI V, LOHMANN E, THOBOIS S, POLLAK P, AGID Y, HEUTINK P, DURR A, BRICE A, FRENCH PARKINSON'S DISEASE GENETICS STUDY GROUP, DE MICHELE, GIUSEPPE, Ibanez, P, DE MICHELE, Giuseppe, Bonifati, V, Lohmann, E, Thobois, S, Pollak, P, Agid, Y, Heutink, P, Durr, A, Brice, A, and FRENCH PARKINSON'S DISEASE GENETICS STUDY, Group

Published
2003

97. How much phenotypic variation can be attributed to parkin genotype?

Author

LOHMANN E, PERIQUET M, BONIFATI V, WOOD NW, BONNET AM, FRAIX V, BROUSSOLLE E, HORSTINK MW, VIDAILHET M, VERPILLAT P, GASSER T, NICHOLL D, TEIVE H, RASKIN S, RASCOL O, DESTEE A, RUBERG M, GASPARINI F, MECO G, AGID Y, DURR A, BRICE A, FRENCH PARKINSON'S DISEASE GENETICS STUDY GROUP, EUROPEAN CONSORTIUM ON GENETIC SUSCEPTIBILITY IN PARKINSON'S DISEASE, DE MICHELE, GIUSEPPE, Lohmann, E, Periquet, M, Bonifati, V, Wood, Nw, DE MICHELE, Giuseppe, Bonnet, Am, Fraix, V, Broussolle, E, Horstink, Mw, Vidailhet, M, Verpillat, P, Gasser, T, Nicholl, D, Teive, H, Raskin, S, Rascol, O, Destee, A, Ruberg, M, Gasparini, F, Meco, G, Agid, Y, Durr, A, Brice, A, FRENCH PARKINSON'S DISEASE GENETICS STUDY, Group, and EUROPEAN CONSORTIUM ON GENETIC SUSCEPTIBILITY IN PARKINSON'S, Disease

Published
2003

100. Association between early-onset Parkinson's disease and parkin gene mutations

Author

LÜCKING CB, DÜRR A, BONIFATI V, VAUGHAN J, GASSER T, HARHANGI BS, MECO G, DENèFLE P, WOOD NW, AGID Y, BRICE A., DE MICHELE, GIUSEPPE, Lücking, Cb, Dürr, A, Bonifati, V, Vaughan, J, DE MICHELE, Giuseppe, Gasser, T, Harhangi, B, Meco, G, Denèfle, P, Wood, Nw, Agid, Y, and Brice, A.

Published
2000

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