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Journal articles on the topic 'Parkinson Diseases'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Zhunina, Olga A., Nikita G. Yabbarov, Andrey V. Grechko, Shaw-Fang Yet, Igor A. Sobenin, and Alexander N. Orekhov. "Neurodegenerative Diseases Associated with Mitochondrial DNA Mutations." Current Pharmaceutical Design 26, no. 1 (February 25, 2020): 103–9. http://dx.doi.org/10.2174/1381612825666191122091320.

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Mitochondrial dysfunction underlies several human chronic pathologies, including cardiovascular disorders, cancers and neurodegenerative diseases. Impaired mitochondrial function associated with oxidative stress can be a result of both nuclear and mitochondrial DNA (mtDNA) mutations. Neurological disorders associated with mtDNA mutations include mitochondrial encephalomyopathy, chronic progressive external ophthalmoplegia, neurogenic weakness, and Leigh syndrome. Moreover, mtDNA mutations were shown to play a role in the development of Parkinson and Alzheimer’s diseases. In this review, current knowledge on the distribution and possible roles of mtDNA mutations in the onset and development of various neurodegenerative diseases, with special focus on Parkinson’s and Alzheimer’s diseases has been discussed.

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Leupold, Dieter, Lukasz Szyc, Goran Stankovic, Sabrina Strobel, Hans-Ullrich Völker, Ulrike Fleck, Thomas Müller, Matthias Scholz, Peter Riederer, and Camelia-Maria Monoranu. "Melanin and Neuromelanin Fluorescence Studies Focusing on Parkinson’s Disease and Its Inherent Risk for Melanoma." Cells 8, no. 6 (June 15, 2019): 592. http://dx.doi.org/10.3390/cells8060592.

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Parkinson’s disease is associated with an increased risk of melanoma (and vice versa). Several hypotheses underline this link, such as pathways affecting both melanin and neuromelanin. For the first time, the fluorescence of melanin and neuromelanin is selectively accessible using a new method of nonlinear spectroscopy, based on a stepwise two-photon excitation. Cutaneous pigmentation and postmortem neuromelanin of Parkinson patients were characterized by fluorescence spectra and compared with controls. Spectral differences could not be documented, implying that there is neither a Parkinson fingerprint in cutaneous melanin spectra nor a melanin-associated fingerprint indicating an increased melanoma risk. Our measurements suggest that Parkinson’s disease occurs without a configuration change of neuromelanin. However, Parkinson patients displayed the same dermatofluorescence spectroscopic fingerprint of a local malignant transformation as controls. This is the first comparative retrospective fluorescence analysis of cutaneous melanin and postmortem neuromelanin based on nonlinear spectroscopy in patients with Parkinson’s disease and controls, and this method is a very suitable diagnostic tool for melanoma screening and early detection in Parkinson patients. Our results suggest a non-pigmentary pathway as the main link between Parkinson’s disease and melanoma, and they do not rule out the melanocortin-1-receptor gene as an additional bridge between both diseases.

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3

Rogaeva, E., and J. Hardy. "Gaucher and Parkinson diseases: Unexpectedly related." Neurology 70, no. 24 (June 9, 2008): 2272–73. http://dx.doi.org/10.1212/01.wnl.0000314657.92762.0f.

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4

Singleton, A. "What does PINK1 mean for Parkinson diseases?" Neurology 63, no. 8 (October 25, 2004): 1350–51. http://dx.doi.org/10.1212/01.wnl.0000144272.53634.49.

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5

NUNOMURA, AKIHIKO, GEORGE PERRY, JING ZHANG, THOMAS J. MONTINE, ATSUSHI TAKEDA, SHIGERU CHIBA, and MARK A. SMITH. "RNA Oxidation in Alzheimer and Parkinson Diseases." Journal of Anti-Aging Medicine 2, no. 3 (January 1999): 227–30. http://dx.doi.org/10.1089/rej.1.1999.2.227.

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6

Okun, M. S., M. R. DeLong, J. Hanfelt, M. Gearing, and A. Levey. "Plasma testosterone levels in Alzheimer and Parkinson diseases." Neurology 62, no. 3 (February 9, 2004): 411–13. http://dx.doi.org/10.1212/01.wnl.0000106840.72938.84.

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7

Zhang, Jing, Izabela Sokal, Elaine R. Peskind, Joseph F. Quinn, Joseph Jankovic, Christopher Kenney, Kathryn A. Chung, Steven P. Millard, John G. Nutt, and Thomas J. Montine. "CSF Multianalyte Profile Distinguishes Alzheimer and Parkinson Diseases." American Journal of Clinical Pathology 129, no. 4 (April 2008): 526–29. http://dx.doi.org/10.1309/w01y0b808emeh12l.

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8

Tennigkeit, Jenny, Tim Feige, Maria Haak, Carina Hellqvist, Ümran S. Seven, Elke Kalbe, Jaqueline Schwarz, et al. "Structured Care and Self-Management Education for Persons with Parkinson’s Disease: Why the First Does Not Go without the Second—Systematic Review, Experiences and Implementation Concepts from Sweden and Germany." Journal of Clinical Medicine 9, no. 9 (August 28, 2020): 2787. http://dx.doi.org/10.3390/jcm9092787.

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Integrated care is regarded as a key for care delivery to persons with chronic long-term conditions such as Parkinson’s disease. For persons with Parkinson’s disease, obtaining self-management support is a top priority in the context of integrated care. Self-management is regarded as a crucial competence in chronic diseases since the affected persons and their caregivers inevitably take up the main responsibility when it comes to day-to-day management. Formal self-management education programs with the focus on behavioral skills relevant to the induction and maintenance of behavioral change have been implemented as a standard in many chronic long-term conditions. However, besides the example of the Swedish National Parkinson School, the offers for persons with Parkinson’s disease remain fragmented and limited in availability. Today, no such program is implemented as a nationwide standard in Germany. This paper provides (1) a systematic review on structured self-management education programs specifically designed or adopted for persons with Parkinson’s disease, (2) presents the Swedish National Parkinson School as an example for a successfully implemented nationwide program and (3) presents a concept for the design, evaluation and long-term implementation of a future-orientated self-management education program for persons with Parkinson’s disease in Germany.

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OJ, Castejón, Carrero Gonzalez CM, and Lastre G. "Diabetes and Neurologic Diseases in a Developing Country." Journal of Clinical Case Studies Reviews & Reports 2, no. 4 (August 31, 2020): 1–7. http://dx.doi.org/10.47363/jccsr/2020(2)141.

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In the present clinical and observational study we have analyzed sixteen patients with type II diabetes, ranging from 56 to 88 years-old., and showing blood hypertension (84%) %), cardiovascular diseases (43%), memory disorder (43%), Parkinson disease (31%), Headaches (25%),. Sleep disorders (18%), gait disturbances (18%), language disorders (18%), dizziness and vertigo (12%), cervicogenic headache (12%) liver diseases (12%), gastrointestinal disease (12%) arthritis (12%), respiratory diseases (6%), Alzheimer disease (6%), and previous cerebrovascular accident (6%). We have diagnosed six mixed syndromes of diabetes and Parkinson disease (37%), three patients with diabetes and Alzheimer disease (18%) two cases with diabetes, blood hypertension and Alzheimer disease (12%) and two case with diabetes and cervicogenic headaches (12%). The pathophysiological mechanisms involved are described in each case. A relationship of diabetic patient lifestyle with environmental conditions, low socioeconomic status and family history is postulated.

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10

Toovey, Stephen, Susan S. Jick, and Christoph R. Meier. "Parkinson’s disease or Parkinson symptoms following seasonal influenza." Influenza and Other Respiratory Viruses 5, no. 5 (March 21, 2011): 328–33. http://dx.doi.org/10.1111/j.1750-2659.2011.00232.x.

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11

Felix da Silva, Caroline, Graziele Estevo Azevedo, and Natália Franco Taketani. "MICROBIOTA INTESTINAL RELACIONADA A DOENÇA DE PARKINSON." Revista Ensaios Pioneiros 5, no. 1 (August 18, 2021): 49–60. http://dx.doi.org/10.24933/rep.v5i1.235.

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RESUMO. A Doença de Parkinson é uma doença crônica, neurodegenerativa e progressiva onde não tem cura. Ainda há muitas investigações para se descobrir a causa da patologia. Em estudos recentes descobriram que pode ter uma relação direta com intestino, com a possibilidade de origem na microbiota intestinal e espalhando-se até o cérebro, com relação a uma desregulação no trato gastrointestinal. É reconhecido que, antes de aparecer os sinais e sintomas motores da doença, o organismo começa a sofrer alterações desde cedo, como a constipação intestinal, com o fortalecimento da hipótese de que a doença de Parkinson tenha início no trato gastrointestinal, e chegue até o cérebro através do nervo vago. Este trabalho pretende abordar sobre a microbiota intestinal e a sua conexão com a doença de Parkinson fazendo revisão de estudos e evidência de como sua composição no hospedeiro pode influenciar o seu metabolismo. A modulação da microbiota intestinal poderá, então, ser uma estratégia para o desenvolvimento de novas opções terapêuticas para o tratamento de doenças neurodegenerativas. ABSTRACT. Parkinson's Disease is a chronic, neurodegenerative and progressive disease that has no cure. There are still many investigations to discover the cause of the pathology. In recent studies they found that it may have a direct relationship with the intestine, with the possibility of originating in the intestinal microbiota and spreading to the brain, with respect to dysregulation in the gastrointestinal tract. It is recognized that, before the appearance of the motor signs and symptoms of the disease, the body begins to undergo changes from an early age, such as intestinal constipation, with the strengthening of the hypothesis that Parkinson's disease starts in the gastrointestinal tract and reaches the brain through the vagus nerve. This work intends to approach the intestinal microbiota and its connection with Parkinson's disease, reviewing studies and evidence on how its composition in the host can influence its metabolism. The modulation of the intestinal microbiota could then be a strategy for the development of new therapeutic options for the treatment of neurodegenerative diseases.

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12

Mahurin, Roderick K., and Francis J. Pirozzolo. "Application of Hick's Law of Response Speed in Alzheimer and Parkinson Diseases." Perceptual and Motor Skills 77, no. 1 (August 1993): 107–13. http://dx.doi.org/10.2466/pms.1993.77.1.107.

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Reaction time in normal subjects is known to increase in a log-linear fashion relative to the number of alternative choices. However, this relationship (formalized as “Hick's law”) has received limited investigation in populations with neurological cognitive impairment. The present study used timed sorting of standard playing cards to test Hick's law for 20 young control subjects, and 20 each of age-matched elderly subjects with Alzheimer disease, Parkinson disease, and no cognitive abnormalities. Although Parkinson patients were slowest in the simple tasks of dealing out the cards and sorting by color, Alzheimer patients showed the greatest slowing for the more cognitively complex conditions of sorting by suit and rank of the cards. The performance of all four groups followed Hick's law in displaying a significant linear relationship between response time and log2 of the number of choices. These findings suggest that, although limitations of information-processing speed in Alzheimer and Parkinson disease affected choice response time, there may be sparing of fundamental cognitive organization in these disorders.

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13

Irwin, Michael H., Walter H. Moos, Douglas V. Faller, Kosta Steliou, and Carl A. Pinkert. "Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases." Drug Development Research 77, no. 3 (February 21, 2016): 109–23. http://dx.doi.org/10.1002/ddr.21294.

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14

Witoelar, Aree, Iris E. Jansen, Yunpeng Wang, Rahul S. Desikan, J. Raphael Gibbs, Cornelis Blauwendraat, Wesley K. Thompson, et al. "Genome-wide Pleiotropy Between Parkinson Disease and Autoimmune Diseases." JAMA Neurology 74, no. 7 (July 1, 2017): 780. http://dx.doi.org/10.1001/jamaneurol.2017.0469.

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15

Heintz, Nathanial, and Huda Zoghbi. "α-synuclein—a link between Parkinson and Alzheimer diseases?" Nature Genetics 16, no. 4 (August 1997): 325–27. http://dx.doi.org/10.1038/ng0897-325.

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16

Hall, Taryn O., Jia Y. Wan, Ignacio F. Mata, Kathleen F. Kerr, Katherine W. Snapinn, Ali Samii, John W. Roberts, Pinky Agarwal, Cyrus P. Zabetian, and Karen L. Edwards. "Risk prediction for complex diseases: application to Parkinson disease." Genetics in Medicine 15, no. 5 (December 6, 2012): 361–67. http://dx.doi.org/10.1038/gim.2012.109.

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17

Theodoulou, G., G. Milner, and A. Jumaian. "Neuroleptics and family history of Parkinson diseases: case report." Eastern Mediterranean Health Journal 7, no. 3 (September 15, 2001): 559–61. http://dx.doi.org/10.26719/2001.7.3.559.

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18

Tóth, Adrián, and Annamária Takáts. "Covid-19 és a Parkinson-kór." Lege Artis Medicinae 31, no. 5-6 (2021): 201–5. http://dx.doi.org/10.33616/lam.31.014.

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Parkinson’s disease is the elderly people’s condition which increases the risk of infections in the upper airways in its advanced stages. Specific diseases (as hypertension, diabetes mellitus), older age and the male sex are significantly worsening the course of COVID-19. It would be challenging to examine parallel these diseases, since they are raising two important questions. First, if Parkinson’s disease be a risk factor of COVID-19 morbidity and mortality. Secondly, how the COVID-19 pandemic can influence the Parkinson’s disease patients. The authors are seeking answers to these questions based on the published results in the topic concerned.

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19

Andrade, Larissa Pires de, Natália Madalena Rinaldi, Flávia Gomes de Melo Coelho, Kátia Tanaka, Florindo Stella, and Lilian Teresa Bucken Gobbi. "Dual task and postural control in Alzheimer's and Parkinson's disease." Motriz: Revista de Educação Física 20, no. 1 (March 2014): 78–84. http://dx.doi.org/10.1590/s1980-65742014000100012.

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Patients with neurodegenerative diseases are required to use cognitive resources while maintaining postural control. The aim of this study was to investigate the effects of a frontal cognitive task on postural control in patients with Alzheimer, Parkinson and controls. Thirty-eight participants were instructed to stand upright on a force platform in two experimental conditions: single and dual task. Participants with Parkinson's disease presented an increase in the coefficient of variation greater than 100% in the dual task as compared to the single task for center of pressure (COP) area and COP path. In addition, patients with Parkinson's and Alzheimer's disease had a higher number of errors during the execution of the cognitive task when compared to the group of elderly without neurodegenerative diseases. The motor cortex, which is engaged in postural control, does not seem to compete with frontal brain regions in the performance of the cognitive task. However, patients with Parkinson's and Alzheimer's disease presented worsened performance in cognitive task.

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20

Orsini, A., N. A. Fragassi, L. Chiacchio, A. M. Falanga, C. Cocchiaro, and D. Grossi. "Verbal and Spatial Memory Span in Patients with Extrapyramidal Diseases." Perceptual and Motor Skills 65, no. 2 (October 1987): 555–58. http://dx.doi.org/10.2466/pms.1987.65.2.555.

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Spatial span (Corsi's block-tapping test) and verbal span (Wechsler's Digits Forward test) were measured in 651 normal subjects and in three groups of extrapyramidal patients (Progressive supranuclear palsy, Parkinson, and Huntington's Chorea). Analysis showed Huntington's Chorea patients scored lower on both tests than did controls and other groups.

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21

Newhouse, Paul A., Alexandra Potter, and Edward D. Levin. "Nicotinic System Involvement in Alzheimer??s and Parkinson??s Diseases." Drugs & Aging 11, no. 3 (September 1997): 206–28. http://dx.doi.org/10.2165/00002512-199711030-00005.

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22

Rossi, Carlo, Duccio Volterrani, Valentina Nicoletti, Gianpiero Manca, Daniela Frosini, Lorenzo Kiferle, Elisa Unti, Paola De Feo, Ubaldo Bonuccelli, and Roberto Ceravolo. "“Parkinson-dementia” diseases: A comparison by double tracer SPECT studies." Parkinsonism & Related Disorders 15, no. 10 (December 2009): 762–66. http://dx.doi.org/10.1016/j.parkreldis.2009.05.012.

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23

Lleó, Alberto, Enrica Cavedo, Lucilla Parnetti, Hugo Vanderstichele, Sanna Kaisa Herukka, Niels Andreasen, Roberta Ghidoni, et al. "Cerebrospinal fluid biomarkers in trials for Alzheimer and Parkinson diseases." Nature Reviews Neurology 11, no. 1 (December 16, 2014): 41–55. http://dx.doi.org/10.1038/nrneurol.2014.232.

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24

Tugcu, Betul, Arif Melikov, Gulsen Babacan Yildiz, Elif Gökcal, Rukiye Ercan, Omer Uysal, and Hakan Ozdemir. "Evaluation of retinal alterations in Parkinson disease and tremor diseases." Acta Neurologica Belgica 120, no. 1 (November 2, 2019): 107–13. http://dx.doi.org/10.1007/s13760-019-01228-x.

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Mosaleva, E. I., I. M. Zhumzhanov, P. V. Alekseenko, S. B. Ismailova, and S. V. Prokopenko. "Cognitive fluctuations associated with therapy in patients with Parkinson diseases." Siberian Medical Review, no. 1 (2021): 63–67. http://dx.doi.org/10.20333/2500136-2021-1-63-67.

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The aim of the research is the assessment of cognitive status dynamics during levodopa pharmacotherapy. Material and methods. A new approach was created to assess cognitive status in patients with PD. It allows diagnosing cognitive fluctuations at an early stage at the highest quality level as well as to correct the disorders rationally and timely. The patients were randomized into two groups. In group 1 (n = 25), the assessment of cognitive status was carried out at the “peak” dose of levodopa and in 6 months at the state of levodopa dose “outcome”. In group 2 (n = 25), respectively, on the contrary, the initial assessment of cognitive status was carried out at the “outcome” of levodopa dose and in 6 months later at the “peak”. The study groups were comparable in terms of such parameters as: age, gender, average duration and stage of disease. On average, all the participants by the study time were at 2.5 stage of the disease according to Hoehn and Yahr scale; and the average length of the disease was 5 years. Results. Th e following statistically signifi cant results were obtained: in the fi rst group (peak–outcome) the average values on MMSE scale at the “peak” were 27 points; at the “outcome” they were – 25; MOCA values were 25 and 22 points, respectively; on FAB scale the values were – 16 and 14.5 points, SCOPA-Cog values were 33 and 28 points. In the second group (outcome – peak), the average values on MMSE scale at the “outcome” were 27, at the “peak” – 28, on MOCA scale – 23 and 25.5, respectively, on FAB scale – 16 and 17.5, SCOPA–Cog – 30 and 33. Conclusion. The present study confi rms that cognitive status of patient associated with antiparkinsonian therapy changes depending on the peak of levodopa and its outcome. At the peak of levodopa action, patients show signifi cantly better results on scaling, and at the end of the day, they demonstrate more significant cognitive impairments. A new two-stage method for assessing CF allows diagnosing cognitive impairments at a better level. Such method is necessary for timely initiation of therapy and rational correction of antiparkinsonian treatment.

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Ota, Miho, Yasuhiro Nakata, Kimiteru Ito, Kouhei Kamiya, Masafumi Ogawa, Miho Murata, Satoko Obu, Hiroshi Kunugi, and Noriko Sato. "Differential Diagnosis Tool for Parkinsonian Syndrome Using Multiple Structural Brain Measures." Computational and Mathematical Methods in Medicine 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/571289.

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Clinical differentiation of parkinsonian syndromes such as the Parkinson variant of multiple system atrophy (MSA-P) and cerebellar subtype (MSA-C) from Parkinson's disease is difficult in the early stage of the disease. To identify the correlative pattern of brain changes for differentiating parkinsonian syndromes, we applied discriminant analysis techniques by magnetic resonance imaging (MRI). T1-weighted volume data and diffusion tensor images were obtained by MRI in eighteen patients with MSA-C, 12 patients with MSA-P, 21 patients with Parkinson’s disease, and 21 healthy controls. They were evaluated using voxel-based morphometry and tract-based spatial statistics, respectively. Discriminant functions derived by step wise methods resulted in correct classification rates of 0.89. When differentiating these diseases with the use of three independent variables together, the correct classification rate was the same as that obtained with step wise methods. These findings support the view that each parkinsonian syndrome has structural deviations in multiple brain areas and that a combination of structural brain measures can help to distinguish parkinsonian syndromes.

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Búřil, Jiří, Petra Búřilová, Andrea Pokorná, Ingrid Kováčová, and Marek Baláž. "Representation of Parkinson's disease and atypical Parkinson's syndromes in the Czech Republic—A nationwide retrospective study." PLOS ONE 16, no. 2 (February 2, 2021): e0246342. http://dx.doi.org/10.1371/journal.pone.0246342.

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Background Parkinson's disease is a progressive neurodegenerative disease which causes health problem that affects more patients in the past few years. To be able to offer appropriate care, epidemiological analyses are crucial at the national level and its comparison with the international situation. Aim The demographic description of reported patients with parkinsonism (including Parkinson's disease and atypical parkinsonian syndromes) according to the International Classification of Diseases (ICD-10) from the national health registries. Methods Retrospective analysis of data available from the National Health Information System–NHIS and the National Registry of Reimbursed Health Services (NRRHS). Analyzed epidemiological data are intending to determine the regional and specific prevalence of Parkinsonism in the Czech Republic. The International Classification of Diseases diagnoses (ICD-10) of G20 (Parkinson’s disease—PD) and G23.1, G23.2, G23.3 (other degenerative disorders of basal ganglia), and G31.8 (another degenerative disease of basal ganglia) from the period of 2012 to 2018 were included into the analysis. Results We identified 78 453 unique patients from national registries in the period 2012 to 2018. Diagnoses of G20, G23.1, G23.2, and G31.8 were registered as the principal diagnoses in 76.6% of all individual patients. Conclusion We have found a growing number of patients coded with ICD-10 of dg. G20, G23.1, G23.2, G23.3, or G31.8 (N = 27 891 in 2012, and N = 30 612 in 2018). We have proven regional differences in the prevalence of Parkinson´s diagnoses. Therefore we assume most likely also differences in the care of patients with PD based on the availability of specialty care centers.

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Moulignier, Antoine, Antoine Gueguen, François-Xavier Lescure, Marc Ziegler, Pierre-Marie Girard, Bernard Cardon, Gilles Pialoux, Jean-Michel Molina, Jean-Philippe Brandel, and Cédric Lamirel. "Does HIV Infection Alter Parkinson Disease?" JAIDS Journal of Acquired Immune Deficiency Syndromes 70, no. 2 (October 2015): 129–36. http://dx.doi.org/10.1097/qai.0000000000000677.

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Turturici, Giuseppina, Gabriella Sconzo, and Fabiana Geraci. "Hsp70 and Its Molecular Role in Nervous System Diseases." Biochemistry Research International 2011 (2011): 1–18. http://dx.doi.org/10.1155/2011/618127.

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Heat shock proteins (HSPs) are induced in response to many injuries including stroke, neurodegenerative disease, epilepsy, and trauma. The overexpression of one HSP in particular, Hsp70, serves a protective role in several different models of nervous system injury, but has also been linked to a deleterious role in some diseases. Hsp70 functions as a chaperone and protects neurons from protein aggregation and toxicity (Parkinson disease, Alzheimer disease, polyglutamine diseases, and amyotrophic lateral sclerosis), protects cells from apoptosis (Parkinson disease), is a stress marker (temporal lobe epilepsy), protects cells from inflammation (cerebral ischemic injury), has an adjuvant role in antigen presentation and is involved in the immune response in autoimmune disease (multiple sclerosis). The worldwide incidence of neurodegenerative diseases is high. As neurodegenerative diseases disproportionately affect older individuals, disease-related morbidity has increased along with the general increase in longevity. An understanding of the underlying mechanisms that lead to neurodegeneration is key to identifying methods of prevention and treatment. Investigators have observed protective effects of HSPs induced by preconditioning, overexpression, or drugs in a variety of models of brain disease. Experimental data suggest that manipulation of the cellular stress response may offer strategies to protect the brain during progression of neurodegenerative disease.

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Pinna, Alessandra, Luca Malfatti, Grazia Galleri, Roberto Manetti, Sara Cossu, Gaia Rocchitta, Rossana Migheli, Pier Andrea Serra, and Plinio Innocenzi. "Ceria nanoparticles for the treatment of Parkinson-like diseases induced by chronic manganese intoxication." RSC Advances 5, no. 26 (2015): 20432–39. http://dx.doi.org/10.1039/c4ra16265j.

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Ceria nanoparticles with controlled size have been studied as antioxidant agents for the in vitro protection of catecholaminergic cells (PC12) exposed to manganese, which is responsible for an occupational form of Parkinson-like disease.

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Trufanov, Y. "Differential diagnosis of Parkinson Disease and Corticobasal Degeneration (disease course and progression)." East European Journal of Neurology, no. 3(21) (September 20, 2018): 44–47. http://dx.doi.org/10.33444/2411-5797.2018.3(21).44-47.

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The objective of our research was the description of the differential diagnostic features of Corticobasal Degeneration and Parkinson Disease in order to improve the diagnosis and the differential diagnosis of these diseases. Corticobasal Degeneration was characterized by marked asymmetry of motor symptoms, malignant progression and the lack of therapeutic effect of dopaminergic medications. Parkinson Disease was characterized by an asymmetry of motor symptoms, benign progression and efficacy of dopaminergic medications.

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Haralur, Satheesh B. "Clinical Strategies for Complete Denture Rehabilitation in a Patient with Parkinson Disease and Reduced Neuromuscular Control." Case Reports in Dentistry 2015 (2015): 1–5. http://dx.doi.org/10.1155/2015/352878.

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The dentist has a large role in geriatric health care for the ever increasing elder population with associated physical and neurological disorders. The Parkinson disease is progressive neurological disorder with resting tremor, bradykinesia, akinesia, and postural instability. The psychological components of disease include depression, anxiety, and cognitive deficiency. Poor oral hygiene, increased susceptibility for dental caries, and periodontal diseases predispose them to early edentulism. The number of Parkinson affected patients visiting dental clinic seeking complete denture is growing. This case report explains the steps involved in the complete denture rehabilitation of Parkinson patient. The effective prosthesis will help in alleviating functional, aesthetic, and psychological disabilities of the patient.

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Alidoust, Leila, and Adele Jafari. "Exosomes: Future Perspective in Neurodegenerative Diseases." Caspian Journal of Neurological Sciences 6, no. 4 (October 1, 2020): 251–58. http://dx.doi.org/10.32598/cjns.6.23.4.

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Neurodegeneration is a progressive and irreversible loss of neuronal cells in specific regions of the brain. Alzheimer Diseases (AD) Parkinson Disease (PD) are the most common forms of neurodegenerative diseases in older people. Exosomes are extracellular nanovesicles that have a key role in physiological processes such as intercellular communication, cell migration, angiogenesis, and anti-tumor immunity. Mounting evidence indicates the role of exosomes in neurodegenerative disorders as possible carriers of disease particles. They have several different potential applications thanks to their unique structure and functions. The present review summarizes recent studies on exosome potentials as a biomarker and therapeutic tool in neurodegenerative diseases. It also provides an overview of the structure and function of exosomes.

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Carvalho, Cristina, Sónia C. Correia, Susana Cardoso, Ana I. Plácido, Emanuel Candeias, Ana I. Duarte, and Paula I. Moreira. "The role of mitochondrial disturbances in Alzheimer, Parkinson and Huntington diseases." Expert Review of Neurotherapeutics 15, no. 8 (June 19, 2015): 867–84. http://dx.doi.org/10.1586/14737175.2015.1058160.

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35

Theocharopoulou, Georgia. "The ubiquitous role of mitochondria in Parkinson and other neurodegenerative diseases." AIMS Neuroscience 7, no. 1 (2020): 43–65. http://dx.doi.org/10.3934/neuroscience.2020004.

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36

Mosquera, I. E., R. Rojas, A. Hernandez, G. Peña, M. Lizarralde, F. Puccio, C. Orellana, et al. "PO24-TH-15 Fibromyalgia associated to Parkinson diseases in Venezuelan patients." Journal of the Neurological Sciences 285 (October 2009): S289—S290. http://dx.doi.org/10.1016/s0022-510x(09)71100-1.

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Espay, Alberto J., Joaquin A. Vizcarra, Luca Marsili, Anthony E. Lang, David K. Simon, Aristide Merola, Keith A. Josephs, et al. "Revisiting protein aggregation as pathogenic in sporadic Parkinson and Alzheimer diseases." Neurology 92, no. 7 (February 11, 2019): 329–37. http://dx.doi.org/10.1212/wnl.0000000000006926.

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The gold standard for a definitive diagnosis of Parkinson disease (PD) is the pathologic finding of aggregated α-synuclein into Lewy bodies and for Alzheimer disease (AD) aggregated amyloid into plaques and hyperphosphorylated tau into tangles. Implicit in this clinicopathologic-based nosology is the assumption that pathologic protein aggregation at autopsy reflects pathogenesis at disease onset. While these aggregates may in exceptional cases be on a causal pathway in humans (e.g., aggregated α-synuclein in SNCA gene multiplication or aggregated β-amyloid in APP mutations), their near universality at postmortem in sporadic PD and AD suggests they may alternatively represent common outcomes from upstream mechanisms or compensatory responses to cellular stress in order to delay cell death. These 3 conceptual frameworks of protein aggregation (pathogenic, epiphenomenon, protective) are difficult to resolve because of the inability to probe brain tissue in real time. Whereas animal models, in which neither PD nor AD occur in natural states, consistently support a pathogenic role of protein aggregation, indirect evidence from human studies does not. We hypothesize that (1) current biomarkers of protein aggregates may be relevant to common pathology but not to subgroup pathogenesis and (2) disease-modifying treatments targeting oligomers or fibrils might be futile or deleterious because these proteins are epiphenomena or protective in the human brain under molecular stress. Future precision medicine efforts for molecular targeting of neurodegenerative diseases may require analyses not anchored on current clinicopathologic criteria but instead on biological signals generated from large deeply phenotyped aging populations or from smaller but well-defined genetic–molecular cohorts.

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Mattis, Paul J., Martin Niethammer, Wataru Sako, Chris C. Tang, Amir Nazem, Marc L. Gordon, Vicky Brandt, Vijay Dhawan, and David Eidelberg. "Distinct brain networks underlie cognitive dysfunction in Parkinson and Alzheimer diseases." Neurology 87, no. 18 (October 5, 2016): 1925–33. http://dx.doi.org/10.1212/wnl.0000000000003285.

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Onyango, Isaac G. "Mitochondria in the pathophysiology of Alzheimer s and Parkinson s diseases." Frontiers in Bioscience 22, no. 5 (2017): 854–72. http://dx.doi.org/10.2741/4521.

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Campbell, M. C., J. Markham, H. Flores, J. M. Hartlein, A. M. Goate, N. J. Cairns, T. O. Videen, and J. S. Perlmutter. "Principal component analysis of PiB distribution in Parkinson and Alzheimer diseases." Neurology 81, no. 6 (July 3, 2013): 520–27. http://dx.doi.org/10.1212/wnl.0b013e31829e6f94.

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Nury, Thomas, Gérard Lizard, and Anne Vejux. "Lipids Nutrients in Parkinson and Alzheimer’s Diseases: Cell Death and Cytoprotection." International Journal of Molecular Sciences 21, no. 7 (April 3, 2020): 2501. http://dx.doi.org/10.3390/ijms21072501.

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Neurodegenerative diseases, particularly Parkinson’s and Alzheimer’s, have common features: protein accumulation, cell death with mitochondrial involvement and oxidative stress. Patients are treated to cure the symptoms, but the treatments do not target the causes; so, the disease is not stopped. It is interesting to look at the side of nutrition which could help prevent the first signs of the disease or slow its progression in addition to existing therapeutic strategies. Lipids, whether in the form of vegetable or animal oils or in the form of fatty acids, could be incorporated into diets with the aim of preventing neurodegenerative diseases. These different lipids can inhibit the cytotoxicity induced during the pathology, whether at the level of mitochondria, oxidative stress or apoptosis and inflammation. The conclusions of the various studies cited are oriented towards the preventive use of oils or fatty acids. The future of these lipids that can be used in therapy/prevention will undoubtedly involve a better delivery to the body and to the brain by utilizing lipid encapsulation.

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Zsolt, Kovacs, Tripon Robert, Nemes Nagy Eniko, Balogh Samarghitan Victor, Tilinca Mariana, Martha Orsolya, and Fazakas Zita. "Arylsulfatase A: An Important Metabolic Factor in Pathophysiology of Different Diseases." Acta Medica Marisiensis 61, no. 3 (September 1, 2015): 233–35. http://dx.doi.org/10.1515/amma-2015-0064.

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Abstract Arylsulfatase A (ARSA) is a lysosomal enzyme that plays an important role in catalysis of degradation of cerebrosidesulphate. The deficiency of this lysosomal enzyme causes an autosomal recessive disorder, called metachromatic leucodystrophy. However, a low ARSA activity can be observed in clinically healthy people, called ARSA pseudodeficiency. In our study we investigated the possible linkage between ARSA activity and sulfatide deficiency causing characteristic aspects of degenerative diseases, such as end stage kidney disease, type 2 Diabetes mellitus, Parkinson syndrome, prostate cancer and HIV (Human Immunodeficiency Virus) infection. We used a spectrophotometric method to determine the activity of ARSA. This method of enzyme dosage is based on a 4 hour long hydrolysis of the ARSA enzyme on 4-nitrocatechol sulfate (p-NCS) substrate. The unit of this measurement is nmol/ml/4h. Our findings show significant values in type 2 diabetes, Parkinson syndrome and chronic kidney disease. The importance of sulfatide in these diseases is well-known, thus presumably the variation of the ARSA’s activity might play an important role in the pathophysiology of these diseases, involving a vicious cycle between sulfatide degradation andthese diseases.

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Liu, Bojing, Fang Fang, Nancy L. Pedersen, Annika Tillander, Jonas F. Ludvigsson, Anders Ekbom, Per Svenningsson, Honglei Chen, and Karin Wirdefeldt. "Vagotomy and Parkinson disease." Neurology 88, no. 21 (April 26, 2017): 1996–2002. http://dx.doi.org/10.1212/wnl.0000000000003961.

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Objective:To examine whether vagotomy decreases the risk of Parkinson disease (PD).Methods:Using data from nationwide Swedish registers, we conducted a matched-cohort study of 9,430 vagotomized patients (3,445 truncal and 5,978 selective) identified between 1970 and 2010 and 377,200 reference individuals from the general population individually matched to vagotomized patients by sex and year of birth with a 40:1 ratio. Participants were followed up from the date of vagotomy until PD diagnosis, death, emigration out of Sweden, or December 31, 2010, whichever occurred first. Vagotomy and PD were identified from the Swedish Patient Register. We estimated hazard ratios (HRs) with 95% confidence intervals (CIs) using Cox models stratified by matching variables, adjusting for country of birth, chronic obstructive pulmonary disease, diabetes mellitus, vascular diseases, rheumatologic disease, osteoarthritis, and comorbidity index.Results:A total of 4,930 cases of incident PD were identified during 7.3 million person-years of follow-up. PD incidence (per 100,000 person-years) was 61.8 among vagotomized patients (80.4 for truncal and 55.1 for selective) and 67.5 among reference individuals. Overall, vagotomy was not associated with PD risk (HR 0.96, 95% CI 0.78–1.17). However, there was a suggestion of lower risk among patients with truncal vagotomy (HR 0.78, 95% CI 0.55–1.09), which may be driven by truncal vagotomy at least 5 years before PD diagnosis (HR 0.59, 95% CI 0.37–0.93). Selective vagotomy was not related to PD risk in any analyses.Conclusions:Although overall vagotomy was not associated the risk of PD, we found suggestive evidence for a potential protective effect of truncal, but not selective, vagotomy against PD development.

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Ahadi, Muhammad Yanuar, Deby Wahyuning Hadi, Soemarno Soemarno, and Evi Octavia. "A Case Report of Parkinson’s Disease in a 70 year Man With Myasthenia Gravis." Journal of Islamic Pharmacy 5, no. 2 (December 11, 2020): 5–8. http://dx.doi.org/10.18860/jip.v5i2.8813.

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AbstractBackground:. Neurodegenerative diseases such as Parkinson’s disease (PD) have increasing incidence, due to lifespan expansion. The association between PD and Myasthenia Gravis (MG) is uncommon, and so far, since 1987, 26 cases have been reported.Case presentation: This is a report of a 70-year-old man was referred into the hospital with ptosis, disfagia and dispnea. He was diagnosed with Suspected Myasthenia Gravis, Post Stroke Trombotik, Parkinson’s Disease and Hypertension. The patient was admitted to the outpatient unit, received of treatment Pyridostigmine, Clopidogrel, Trihexylphenidil, Vitamine B1, Vitaminie B6, Vitamine B12 and Levodopa-Benserazide .Discussion: Treatment guidelines by using some guidelines are also drug doses and do not have adverse side reactions during treatment.Conclusion:. PD and MG very rarely occur together. case report or a series of brief cases reported in the literature, it is very important not to miss the diagnosis of MG in patients with PD, because the treatment implications are very important and greatly influence the prognosis. More basic research needs to be done to understand the pathogenesis of both diseases, to provide more therapeutic options and possibly change the approach of the patient, whose quality of life is determined by these two neurological diseases, which have an increased impact on increasing disabilityKey words: Parkinson disease; Myasthenia gravis; co‐occurrence; case report.

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Bukvicki, Danka, Davide Gottardi, Sahdeo Prasad, Miroslav Novakovic, Petar D. Marin, and Amit Kumar Tyagi. "The Healing Effects of Spices in Chronic Diseases." Current Medicinal Chemistry 27, no. 26 (July 23, 2020): 4401–20. http://dx.doi.org/10.2174/0929867325666180831145800.

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Spices are not only just herbs used in culinary for improving the taste of dishes, they are also sources of a numerous bioactive compounds significantly beneficial for health. They have been used since ancient times because of their antimicrobial, anti-inflammatory and carminative properties. Several scientific studies have suggested their protective role against chronic diseases. In fact, their active compounds may help in arthritis, neurodegenerative disorders (Alzheimer’s, Parkinson, Huntington’s disease, amyotrophic lateral sclerosis, etc.), diabetes, sore muscles, gastrointestinal problems and many more. In the present study, possible roles of spices and their active components, in chronic diseases (cancer, arthritis, cardiovascular diseases, etc.) along with their mechanism of action have been reviewed.

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Korolev, A. G., A. V. Novoseletskaya, and N. M. Kiseleva. "ABNORMALITY IN LEARNING ON THE MODEL OF PARKINSON-LIKE SYNDROME: THE CORRECTABILITY BY THYMUS PEPTIDES." Medical Journal of the Russian Federation 24, no. 6 (December 15, 2018): 310–15. http://dx.doi.org/10.18821/0869-2106-2018-24-6-310-315.

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In recent times the question of the bidirectional interactions of the neuroendocrine and immune systems is studied quite actively, its mechanisms offer the opportunity to allow for optimization the therapy of several diseases, including Parkinson’s disease. The purpose of this work is to study the influence of peptide drugs derived from the body’s immune system, the thymus, for the avoidance test conditioning, both in health and in the model of Parkinson-like syndrome. The work was performed on 80 male Wistar rats weighing 300-350 g. The injection of thymosin fraction 5 and thymalin to animals corrects clinical traits and behavioral dysfunctions caused by the singular injection of the neurotoxin. It also facilitates conditioned active evasion response in rats, which is especially noticeable at the early stages of memory footprint formation.

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Maria, Carrero-González Carmen, Castejón OJ, and Judith Cristina Martínez Royert. "“Clinical Study of Memory Disorders in Aging Patients with Associated Cardiovascular, Neurological, Neurobehavioral and Metabolic Diseases”. A Review." Journal of Clinical Case Studies Reviews & Reports 3, no. 2 (April 30, 2021): 1–9. http://dx.doi.org/10.47363/jccsr/2020(3)167.

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We have observed semantic memory and episodic memory disorders (100%) in patients ranging from 40 to 92 years-old, associated to cardiovascular diseases and blood hypertension (82%), sleep disorders (50%), neurobehavioral disorders (44%), such as depression, anxiety, aggression, and vascular demencia, disorders of language (36%), neurosensory disorders (28%), as diminution of visual and hearing acuity, dizziness (26%), Parkinson disease (34%), Alzheimer disease (21%), gait disturbances (10%), vertigo (10%), cervicalgia and cervicogenic headache (10%) trigeminal neuralgia (2%,), We observed as comorbidities the following non-nervous diseases: metabolic diseases as diabetes (21%) and hypothyroidism (5%), gastrointestinal pathology (21%), such as constipation, loss of sphincter control, and gastritis, arthritis (13%), prostatic hypertrophy (1%) and loss of weight (1%). We consider that according to their high frequency the most risk factors associated to memory disorders are cardiovascular diseases and blood hypertension (82%), sleep disorders (50%), neurobehavioral disorders (44%), such as depression, anxiety, aggression, and vascular demencia, disorders of language (36%), neurosensory disorders (28%), as diminution of visual and hearing acuity, dizziness (26%), and Parkinson disease (34%).

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Junakovic, Alisa, and Srdjana Telarovic. "The effects of art therapy on Parkinson`s and Alzheimer`s disease." Medicina Fluminensis 57, no. 3 (September 1, 2021): 236–43. http://dx.doi.org/10.21860/medflum2021_261184.

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Art therapy is one of the non-pharmacological treatment modalities for many diseases, including neurological and psychiatric disorders. Adrian Hill started art therapy in the 1940s. Parkinson`s disease is one of the progressive neurodegenerative diseases characterized by various motor and non-motor symptoms. As patients with Parkinson`s disease often report low quality of life despite improving their motor symptoms, complementary therapy may reduce their difficulties. Music and dance therapy, clay manipulation therapy, and tai chi training have promising results. There is also art therapy for one of the most common causes of dementia worldwide, Alzheimer`s disease. In addition to standard pharmacological treatment for Alzheimer`s disease e.g. cholinesterase inhibitors, music and visual arts therapy are evolving. This article presented some of the art therapy methods used in the most common neurodegenerative disorders, Parkinson`s and Alzheimer`s. In addition, we also presented some of the limitations of those studies. Some of the limitations are as follows: small sample size, relatively short duration of therapy sessions, and the fact that it is doubtful that art therapy could improve symptoms and cognitive abilities of people with advanced forms of neurodegenerative disorders.

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Richardson, Daniel, Meriel M. McEntagart, and Jeremy D. Isaacs. "DCTN1-related Parkinson-plus disorder (Perry syndrome)." Practical Neurology 20, no. 4 (May 20, 2020): 317–19. http://dx.doi.org/10.1136/practneurol-2020-002505.

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Dynactin-1 (DCTN1)-related Parkinson-plus disorder (Perry syndrome) is an autosomal dominant neurodegenerative disorder characterised by levodopa-resistant parkinsonism, weight loss, mood change and central hypoventilation. Ventilatory insufficiency is the predominant cause of death. It has been previously described in 87 people from 20 families with a worldwide distribution. It is now recognised as a distinct TDP-43 proteinopathy caused by a pathological mutation in DCTN1. Its rarity and clinical overlap with other neurodegenerative diseases increase the risk of delayed or incorrect diagnosis. Ventilatory support can improve life expectancy but this depends upon its recognition; overall its prognosis remains poor. We report a patient with DCTN1-related Parkinson-plus disorder, in whom genetic confirmation came only after death.

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Grespi, Francesca, and Gerry Melino. "P73 and age-related diseases: is there any link with Parkinson Disease?" Aging 4, no. 12 (December 18, 2012): 923–31. http://dx.doi.org/10.18632/aging.100515.

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