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Journal articles on the topic 'Parkinson's disease; Huntington's disease'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

Teräväinen, H., M. Hietanen, J. Stoessl, and D. B. Calne. "Dementia in Movement Disorders." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 13, S4 (November 1986): 546–58. http://dx.doi.org/10.1017/s031716710003729x.

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Abstract:Of all the movement disorders, Huntington's disease has been most consistently associated with dementia, while it is only over the last decade that intellectual and cognitive decline have been recognized as common features of Parkinson's disease. It is now known that the pathology in these two conditions reflects differential involvement of the striatum. The Huntington lesion is primarily in the caudate, while the Parkinson lesion preferentially affects the putamen. Both conditions have more diffuse pathology, and dementia may also occur in a wide range of other extrapyramidal diseases, such as progressive supranuclear palsy, the parkinsonism-dementia complex of Guam, and certain spinocerebellar degenerations. Clinicopathological correlations will be reviewed in these disorders of primarily subcortical pathology, and comparisons will be made with Alzheimer's disease, a disorder of predominantly cortical pathology.

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2

Hague, S. M. "Neurodegenerative disorders: Parkinson's disease and Huntington's disease." Journal of Neurology, Neurosurgery & Psychiatry 76, no. 8 (August 1, 2005): 1058–63. http://dx.doi.org/10.1136/jnnp.2004.060186.

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3

Hanes, K. R., D. G. Andrewes, and C. Pantelis. "Dysfluency in Huntington's disease, Parkinson's disease and schizophrenia." Applied Neuropsychology 2, no. 1 (February 1995): 29–34. http://dx.doi.org/10.1207/s15324826an0201_5.

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4

O’Keeffe, Gráinne C., Andrew W. Michell, and Roger A. Barker. "Biomarkers in Huntington's and Parkinson's Disease." Annals of the New York Academy of Sciences 1180, no. 1 (October 2009): 97–110. http://dx.doi.org/10.1111/j.1749-6632.2009.04943.x.

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5

Ramig, Lorraine A., Ingo R. Titze, Ronald C. Scherer, and Steven P. Ringel. "Acoustic Analysis of Voices of Patients with Neurologic Disease: Rationale and Preliminary Data." Annals of Otology, Rhinology & Laryngology 97, no. 2 (March 1988): 164–72. http://dx.doi.org/10.1177/000348948809700214.

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This paper presents a rationale for acoustic analysis of voices of neurologically diseased patients, and reports preliminary data from patients with myotonic dystrophy, Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis, as well as from individuals at risk for Huntington's disease. Noninvasive acoustic analysis may be of clinical value to the otolaryngologist, neurologist, and speech pathologist for early and differential diagnosis and for documenting disease progression in these various neurologic disorders.

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6

Dimovski, E. B., J. C. Stout, S. A. Wylie, and E. R. Siemers. "Spatial cognitive shifting in huntington's disease and parkinson's disease." Archives of Clinical Neuropsychology 14, no. 1 (January 1, 1999): 126. http://dx.doi.org/10.1093/arclin/14.1.126.

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7

Davies, Katherine M., Julian F. B. Mercer, Nicholas Chen, and Kay L. Double. "Copper dyshomoeostasis in Parkinson's disease: implications for pathogenesis and indications for novel therapeutics." Clinical Science 130, no. 8 (March 8, 2016): 565–74. http://dx.doi.org/10.1042/cs20150153.

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Copper is a biometal essential for normal brain development and function, thus copper deficiency or excess results in central nervous system disease. Well-characterized disorders of disrupted copper homoeostasis with neuronal degeneration include Menkes disease and Wilson's disease but a large body of evidence also implicates disrupted copper pathways in other neurodegenerative disorders, including Parkinson's disease, Alzheimer's disease, Amyotrophic lateral sclerosis, Huntington's disease and prion diseases. In this short review we critically evaluate the data regarding changes in systemic and brain copper levels in Parkinson's disease, where alterations in brain copper are associated with regional neuronal cell death and disease pathology. We review copper regulating mechanisms in the human brain and the effects of dysfunction within these systems. We then examine the evidence for a role for copper in pathogenic processes in Parkinson's disease and consider reports of diverse copper-modulating strategies in in vitro and in vivo models of this disorder. Copper-modulating therapies are currently advancing through clinical trials for Alzheimer's and Huntington's disease and may also hold promise as disease modifying agents in Parkinson's disease.

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8

Fink, J. Stephen, James M. Schumacher, Samuel L. Ellias, E. Prather Palmer, Marie Saint-Hilaire, Kathleen Shannon, Richard Penn, et al. "Porcine Xenografts in Parkinson's Disease and Huntington's Disease Patients: Preliminary Results." Cell Transplantation 9, no. 2 (March 2000): 273–78. http://dx.doi.org/10.1177/096368970000900212.

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The observation that fetal neurons are able to survive and function when transplanted into the adult brain fostered the development of cellular therapy as a promising approach to achieve neuronal replacement for treatment of diseases of the adult central nervous system. This approach has been demonstrated to be efficacious in patients with Parkinson's disease after transplantation of human fetal neurons. The use of human fetal tissue is limited by ethical, infectious, regulatory, and practical concerns. Other mammalian fetal neural tissue could serve as an alternative cell source. Pigs are a reasonable source of fetal neuronal tissue because of their brain size, large litters, and the extensive experience in rearing them in captivity under controlled conditions. In Phase I studies porcine fetal neural cells grafted unilaterally into Parkinson's disease (PD) and Huntington's disease (HD) patients are being evaluated for safety and efficacy. Clinical improvement of 19% has been observed in the Unified Parkinson's Disease Rating Scale “off” state scores in 10 PD patients assessed 12 months after unilateral striatal transplantation of 12 million fetal porcine ventral mesencephalic (VM) cells. Several patients have improved more than 30%. In a single autopsied PD patient some porcine fetal VM cells were observed to survive 7 months after transplantation. Twelve HD patients have shown a favorable safety profile and no change in total functional capacity score 1 year after unilateral striatal placement of up to 24 million fetal porcine striatal cells. Xenotransplantation of fetal porcine neurons is a promising approach to delivery of healthy neurons to the CNS. The major challenges to the successful use of xenogeneic fetal neuronal cells in neurodegenerative diseases appear to be minimizing immune-mediated rejection, management of the risk of xenotic (cross-species) infections, and the accurate assessment of clinical outcome of diseases that are slowly progressive.

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9

Boecker, H., A. Ceballos-Baumann, P. Bartenstein, A. Weindl, H. R. Siebner, T. Fassbender, F. Munz, M. Schwaiger, and B. Conrad. "Sensory processing in Parkinson's and Huntington's disease." Brain 122, no. 9 (September 1999): 1651–65. http://dx.doi.org/10.1093/brain/122.9.1651.

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10

Ludlow, Christy L., Nadine P. Connor, and Celia J. Bassich. "Speech timing in Parkinson's and Huntington's disease." Brain and Language 32, no. 2 (November 1987): 195–214. http://dx.doi.org/10.1016/0093-934x(87)90124-6.

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11

Hanes, Karl R. "Brief Report: Bradyphrenia in Parkinson's Disease, Huntington's Disease, and Schizophrenia." Cognitive Neuropsychiatry 1, no. 2 (May 1996): 165–70. http://dx.doi.org/10.1080/135468096396622.

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12

Flint Beal, M., and Clifford W. Shults. "Effects of Coenzyme Q10in Huntington's disease and early Parkinson's disease." BioFactors 18, no. 1-4 (2003): 153–61. http://dx.doi.org/10.1002/biof.5520180218.

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13

Bernard-Gauthier, Vadim, Justin J. Bailey, Arturo Aliaga, Alexey Kostikov, Pedro Rosa-Neto, Melinda Wuest, Garrett M. Brodeur, Barry J. Bedell, Frank Wuest, and Ralf Schirrmacher. "Development of subnanomolar radiofluorinated (2-pyrrolidin-1-yl)imidazo[1,2-b]pyridazine pan-Trk inhibitors as candidate PET imaging probes." MedChemComm 6, no. 12 (2015): 2184–93. http://dx.doi.org/10.1039/c5md00388a.

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Dysregulation of tropomyosin receptor kinases (TrkA/B/C) expression and signalling is recognized as a hallmark of numerous neurodegenerative diseases including Parkinson's, Huntington's and Alzheimer's disease.

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14

Millan, Sabera, Lakkoji Satish, Krishnendu Bera, and Harekrushna Sahoo. "Binding and inhibitory effect of the food colorants Sunset Yellow and Ponceau 4R on amyloid fibrillation of lysozyme." New Journal of Chemistry 43, no. 9 (2019): 3956–68. http://dx.doi.org/10.1039/c8nj05827j.

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Amyloid fibrillogenesis of proteins is known to be the root cause of a large number of diseases like Parkinson's, Alzheimer's, and Huntington's disease, spongiform encephalopathy, amyloid polyneuropathy, type-II diabetes, etc.

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15

Hulvershorn, L. A., J. C. Stout, J. S. Paulsen, and E. Siemers. "Frontal neuropsychiatric syndromes in Huntington's disease (HD) and Parkinson's disease (PD)." Archives of Clinical Neuropsychology 14, no. 1 (January 1, 1999): 133. http://dx.doi.org/10.1093/arclin/14.1.133.

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16

Watson, Daniel L., Celia L. Carpenter, Shelley S. Marks, and David A. Greenberg. "Striatal calcium channel antagonist receptors in huntington's disease and parkinson's disease." Annals of Neurology 23, no. 3 (March 1988): 303–5. http://dx.doi.org/10.1002/ana.410230316.

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17

Henderson, Tracy, Nellie Georgiou-Karistianis, Owen White, Lynette Millist, David R. Williams, Andrew Churchyard, and Joanne Fielding. "Inhibitory control during smooth pursuit in Parkinson's disease and Huntington's disease." Movement Disorders 26, no. 10 (May 31, 2011): 1893–99. http://dx.doi.org/10.1002/mds.23757.

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18

Ferrer, I., R. Blanco, B. Cutillas, and S. Ambrosio. "Fas and Fas-L expression in Huntington's disease and Parkinson's disease." Neuropathology and Applied Neurobiology 26, no. 5 (October 2000): 424–33. http://dx.doi.org/10.1046/j.1365-2990.2000.00267.x.

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19

Jones, Dean L., James G. Phillips, John L. Bradshaw, Robert Iansek, and Judy A. Bradshaw. "Programming of single movements in Parkinson's disease: Comparison with huntington's disease." Journal of Clinical and Experimental Neuropsychology 14, no. 5 (September 1992): 762–72. http://dx.doi.org/10.1080/01688639208402861.

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20

Lopez, William Omar Contreras, Guido Nikkhah, Ulf D. Kahlert, Donata Maciaczyk, Tomasz Bogiel, Sven Moellers, Elisabeth Schültke, Máté Döbrössy, and Jaroslaw Maciaczyk. "Clinical neurotransplantation protocol for Huntington's and Parkinson's disease." Restorative Neurology and Neuroscience 31, no. 5 (2013): 579–95. http://dx.doi.org/10.3233/rnn-130317.

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21

Outeiro, T. F. "From Mad Cows to Neurotic Yeast: Novel Molecular Approaches to Understand Neurodegeneration." Microscopy and Microanalysis 14, S3 (September 2008): 105–6. http://dx.doi.org/10.1017/s143192760808954x.

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Aging is the major known risk factor for Alzheimer's disease (AD) and Parkinson's disease (PD), but genetic deffects have been associated with familial cases. Huntington's disease (HD) is a purely genetic neurodegenerative disorder, where mutations in the IT15 gene, encoding for the protein huntingtin, determine the development of the disease. The Prion diseases differ from these other disorders because they can also have infections origin.

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22

Hanes, Karl R., David G. Andrewes, and Christos Pantelis. "Cognitive flexibility and complex integration in Parkinson's disease, Huntington's disease, and Schizophrenia." Journal of the International Neuropsychological Society 1, no. 6 (November 1995): 545–53. http://dx.doi.org/10.1017/s1355617700000679.

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AbstractTwo new tasks designed to individualize and assess aspects of cognitive flexibility and complex integration were administered to patients with schizophrenia (n = 16), Parkinson's disease (PD; n = 25) and Huntington's disease (HD; n = 12). Findings indicated impaired performance in the schizophrenic and HD groups on components of solution fluency, reactive flexibility and integration. The PD group demonstrated normal performance on all but the solution fluency and reaction time measures. These findings corroborate previous studies suggesting that executive and problem solving disturbances feature in schizophrenia and HD and that these functions may not be as severely affected in medicated PD. Slowed reaction time by both dementia groups is explained with reference to the concept of bradyphrenia. (JINS, 1995, 1, 545–553.)

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23

Hanes, Karl R., David G. Andrewes, Christos Pantelis, and Edmond Chiu. "Subcortical dysfunction in schizophrenia: a comparison with Parkinson's disease and Huntington's disease." Schizophrenia Research 19, no. 2-3 (May 1996): 121–28. http://dx.doi.org/10.1016/0920-9964(95)00069-0.

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24

Schapira, Anthony H. V., C. Warren Olanow, J. Timothy Greenamyre, and Erwan Bezard. "Slowing of neurodegeneration in Parkinson's disease and Huntington's disease: future therapeutic perspectives." Lancet 384, no. 9942 (August 2014): 545–55. http://dx.doi.org/10.1016/s0140-6736(14)61010-2.

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25

AGOSTINO, R., A. BERARDELLI, A. FORMICA, N. ACCORNERO, and M. MANFREDI. "SEQUENTIAL ARM MOVEMENTS IN PATIENTS WITH PARKINSON'S DISEASE, HUNTINGTON'S DISEASE AND DYSTONIA." Brain 115, no. 5 (1992): 1481–95. http://dx.doi.org/10.1093/brain/115.5.1481.

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26

Allen, E., R. Saatchi, B. Jervis, S. Oke, N. Hudson, and M. Grimsley. "Computerised EEG methods for the diagnosis of huntington's disease and Parkinson's disease." Electroencephalography and Clinical Neurophysiology 87, no. 2 (August 1993): S33. http://dx.doi.org/10.1016/0013-4694(93)90978-5.

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27

Diederich, Nico J., and Christopher G. Goetz. "Neuropsychological and Behavioral Aspects of Transplants in Parkinson's Disease and Huntington's Disease." Brain and Cognition 42, no. 2 (March 2000): 294–306. http://dx.doi.org/10.1006/brcg.1999.1105.

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28

Liu, He, and Ni Song. "Molecular Mechanism of Adult Neurogenesis and its Association with Human Brain Diseases." Journal of Central Nervous System Disease 8 (January 2016): JCNSD.S32204. http://dx.doi.org/10.4137/jcnsd.s32204.

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Recent advances in neuroscience challenge the old dogma that neurogenesis occurs only during embryonic development. Mounting evidence suggests that functional neurogenesis occurs throughout adulthood. This review article discusses molecular factors that affect adult neurogenesis, including morphogens, growth factors, neurotransmitters, transcription factors, and epigenetic factors. Furthermore, we summarize and compare current evidence of associations between adult neurogenesis and human brain diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and brain tumors.

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29

Beal, M. Flint. "Oxidative Damage in Neurodegenerative Diseases." Neuroscientist 3, no. 1 (January 1997): 21–27. http://dx.doi.org/10.1177/107385849700300112.

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Increasing evidence has implicated oxidative damage in the pathogenesis of neurodegenerative diseases. The major source of free radicals in the cell is the mitochondria. Peroxynitrite is formed by the reaction of superoxide with nitric oxide, and it produces both oxidative damage and protein nitration. Mutations in CuZn superoxide dismutase associated with familial ALS may result in increased −OH radical generation or in increased reactivity with peroxynitrite to nitrate proteins. There is evidence for increased oxidative damage in Alzheimer's disease and Parkinson's disease in neurons undergoing neurodegenerative changes. A role for oxidative damage in Parkinson's disease toxicity and in Huntington's disease is supported by studies in animal models. Improved antioxidant therapies may prove useful in slowing or halting the progression of neurodegenerative diseases.

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30

Reynolds, Gavin P., Ruth M. Boulton, Sally J. Pearson, Alan L. Hudson, and David J. Nutt. "Imidazoline binding sites in Huntington's and Parkinson's disease putamen." European Journal of Pharmacology 301, no. 1-3 (April 1996): R19—R21. http://dx.doi.org/10.1016/0014-2999(96)00196-3.

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31

Emser, W., M. Brenner, T. Stober, and K. Schimrigk. "Changes in nocturnal sleep in Huntington's and Parkinson's disease." Journal of Neurology 235, no. 3 (January 1988): 177–79. http://dx.doi.org/10.1007/bf00314313.

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32

STOUT, JULIE C., WILLIAM C. RODAWALT, and ERIC R. SIEMERS. "Risky decision making in Huntington's disease." Journal of the International Neuropsychological Society 7, no. 1 (January 2001): 92–101. http://dx.doi.org/10.1017/s1355617701711095.

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In the clinical setting, Huntington's disease is associated with problems in judgment and decision making, however, the extent of these problems and their association with clinical characteristics have not been assessed. Recently, a laboratory-based simulated gambling task has been used to quantify similar decision-making deficits in ventromedial frontal lobe damaged participants. We hypothesized that participants with Huntington's disease (HD) would show deficits on this gambling task. For this study, 14 HD participants were asked to make 100 selections from four decks of cards with varied payoffs in order to maximize winnings of play money. They were compared to 22 participants with Parkinson's disease (PD) and 33 healthy controls. After an initial period in which participants had to learn contingencies of the decks, the HD group made fewer advantageous selections than the PD and control groups. In HD, the number of advantageous selections in the gambling task was correlated with measures of memory and conceptualization but not disinhibition. Thus, people with HD may have had difficulties learning or remembering win/loss contingencies of the decks, or they may have failed to consistently take these into account in their card selections. These findings are consistent with current models of frontal-subcortical brain circuits and behavior. (JINS, 2001, 7, 92–101.)

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33

Roos, R. A. C., J. M. C. Steenvoorden, G. J. Mulder, and G. M. J. Van Kempen. "Acetaminophen sulfation in patients with Parkinson's disease or Huntington's disease is not impaired." Neurology 43, no. 7 (July 1, 1993): 1373. http://dx.doi.org/10.1212/wnl.43.7.1373.

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34

Stout, Julie C., Scott A. Wylie, Patricia M. Simone, and Eric R. Siemers. "Influence of Competing Distractors on Response Selection in Huntington's Disease and Parkinson's Disease." Cognitive Neuropsychology 18, no. 7 (September 2001): 643–53. http://dx.doi.org/10.1080/02643290126376.

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35

Diguet, Elsa, Pierre-Olivier Fernagut, Xing Wei, Yansheng Du, Richard Rouland, Christian Gross, Erwan Bezard, and François Tison. "Deleterious effects of minocycline in animal models of Parkinson's disease and Huntington's disease." European Journal of Neuroscience 19, no. 12 (June 2004): 3266–76. http://dx.doi.org/10.1111/j.0953-816x.2004.03372.x.

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36

Sahoo, Abhilash, and Silvina Matysiak. "Computational insights into lipid assisted peptide misfolding and aggregation in neurodegeneration." Physical Chemistry Chemical Physics 21, no. 41 (2019): 22679–94. http://dx.doi.org/10.1039/c9cp02765c.

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37

Bombardi Duarte, Ana Carolina, Maycon Giovani Santana, Guilherme di Camilo Orfali, Carlos Tadeu Parisi de Oliveira, and Denise Goncalves Priolli. "Literature Evidence and ARRIVE Assessment on Neuroprotective Effects of Flavonols in Neurodegenerative Diseases' Models." CNS & Neurological Disorders - Drug Targets 17, no. 1 (April 26, 2018): 34–42. http://dx.doi.org/10.2174/1871527317666171221110139.

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Background and Objective: This paper was based on a literature search of PubMed and Scielo databases using the keywords “Flavonoids, Neuroprotection, Quercetin, Rutin, Isoquercitrin, Alzheimer, Parkinson, Huntington” and combinations of all the words. Method: We collected relevant publications, during the period of 2000 to 2016, emphasizing in vivo and in vitro studies with neurological assessment of flavonol's potentials, as well as classifying studies according to evidence levels, in order to elucidate evidence-based literature and its application on clinical research. In addition, we highlight the importance of flavonols in modern research fields, indicating their neuroprotective potential and use thereof as preventive and therapeutic treatment of numerous neurodegenerative disease. Neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and Huntington's disease, represent worldwide a major health problem with great financial impact. They are multifactorial diseases, hallmarked by similar pathogenesis that covers conditions such as oxidative stress, formation of free radicals, abnormal protein dynamics (degradation and aggregation), mitochondrial dysfunction, lipid peroxidation and cellular death or senescence. Flavonols are polyphenolic compounds, widely distributed in the plant kingdom and found in high concentrations in vegetables, fruits and teas. Their neuroprotective effects are mainly related to their antioxidant, anti-proliferative and anti-inflammatory properties. Conclusion: It was this paper's intention to contribute with an evidence analysis of recent studies approaching neuroprotective effects of flavonols and the potential to conduct human clinical studies.

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38

Griffiths, William J., and Yuqin Wang. "Oxysterol research: a brief review." Biochemical Society Transactions 47, no. 2 (April 1, 2019): 517–26. http://dx.doi.org/10.1042/bst20180135.

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Abstract In the present study, we discuss the recent developments in oxysterol research. Exciting results have been reported relating to the involvement of oxysterols in the fields of neurodegenerative disease, especially in Huntington's disease, Parkinson's disease and Alzheimer's disease; in signalling and development, in particular, in relation to Hedgehog signalling; and in cancer, with a special focus on (25R)26-hydroxycholesterol. Methods for the measurement of oxysterols, essential for understanding their mechanism of action in vivo, and valuable for diagnosing rare diseases of cholesterol biosynthesis and metabolism are briefly considered.

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39

Proudfoot, Owen. "Manganese in manganism, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and Batten disease: A narrative review." Neurology India 65, no. 6 (2017): 1241. http://dx.doi.org/10.4103/0028-3886.217949.

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40

Petrozzi, Lucia, Giulia Ricci, Noemi J. Giglioli, Gabriele Siciliano, and Michelangelo Mancuso. "Mitochondria and Neurodegeneration." Bioscience Reports 27, no. 1-3 (June 13, 2007): 87–104. http://dx.doi.org/10.1007/s10540-007-9038-z.

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Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. However, despite the evidence of morphological, biochemical and molecular abnormalities in mitochondria in various tissues of patients with neurodegenerative disorders, the question “is mitochondrial dysfunction a necessary step in neurodegeneration?” is still unanswered. In this review, we highlight some of the major neurodegenerative disorders (Alzheimer's disease, Parkinson's disease, Amyotrophic lateral sclerosis and Huntington's disease) and discuss the role of the mitochondria in the pathogenetic cascade leading to neurodegeneration.

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41

Ezrin-Waters, Cheryl, and L. Resch. "The Nucleus Basalis of Meynert." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 13, no. 1 (February 1986): 8–14. http://dx.doi.org/10.1017/s0317167100035721.

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ABSTRACT:The nucleus basalis of Meynert has been studied extensively in the recent literature. Interest in this nucleus has resulted from the discovery that it is a major source of cortical cholinergic input and that there is neuronal loss in the nucleus basalis in some dementing illnesses. Consistent and severe involvement of the nucleus basalis of Meynert has been found in Alzheimer's disease and in the dementia accompanying Parkinson's disease. Occasional involvement is present in other dementing illnesses, such as progressive supranuclear palsy, Parkinsonism-Dementia complex of Guam, dementia pugilistica, Pick's disease, Korsakoff's syndrome, Down's Syndrome and Creutzfeldt- Jakob disease. Huntington's disease spares this nucleus. However, the role of the nucleus in cognitive function is as yet undetermined. Even its alteration with normal aging remains controversial. This review details the pathological studies of this region to date, with particular emphasis on the dementias. Its role in the dementias of Alzheimer's disease and Parkinson's disease is specifically addressed.

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42

Daneault, Jean-François, Benoit Carignan, Abbas F. Sadikot, and Christian Duval. "Inter-limb coupling during diadochokinesis in Parkinson's and Huntington's disease." Neuroscience Research 97 (August 2015): 60–68. http://dx.doi.org/10.1016/j.neures.2015.02.009.

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43

Martin, Antonio, Giulia De Vivo, and Vittorio Gentile. "Possible Role of the Transglutaminases in the Pathogenesis of Alzheimer's Disease and Other Neurodegenerative Diseases." International Journal of Alzheimer's Disease 2011 (2011): 1–8. http://dx.doi.org/10.4061/2011/865432.

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Transglutaminases are ubiquitous enzymes which catalyze posttranslational modifications of proteins. Recently, transglutaminase-catalyzed post-translational modification of proteins has been shown to be involved in the molecular mechanisms responsible for human diseases. Transglutaminase activity has been hypothesized to be involved also in the pathogenetic mechanisms responsible for several human neurodegenerative diseases. Alzheimer's disease and other neurodegenerative diseases, such as Parkinson's disease, supranuclear palsy, Huntington's disease, and other polyglutamine diseases, are characterized in part by aberrant cerebral transglutaminase activity and by increased cross-linked proteins in affected brains. This paper focuses on the possible molecular mechanisms by which transglutaminase activity could be involved in the pathogenesis of Alzheimer's disease and other neurodegenerative diseases, and on the possible therapeutic effects of selective transglutaminase inhibitors for the cure of patients with diseases characterized by aberrant transglutaminase activity.

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44

FURLONG, Robert A., Yolanda NARAIN, Julia RANKIN, Andreas WYTTENBACH, and David C. RUBINSZTEIN. "α-Synuclein overexpression promotes aggregation of mutant huntingtin." Biochemical Journal 346, no. 3 (March 7, 2000): 577–81. http://dx.doi.org/10.1042/bj3460577.

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Protein aggregates are a neuropathological feature of Huntington's disease and Parkinson's disease. Mutant huntingtin exon 1 with 72 CAG repeats fused to enhanced green fluorescent protein (EGFP) forms hyperfluorescent inclusions in PC12 cells. Inclusion formation is enhanced in cells co-transfected with EGFP-huntingtin-(CAG)72 and α-synuclein, a major component of Parkinson's disease aggregates. However, α-synuclein does not form aggregates by itself, nor does it appear in huntingtin inclusions in vitro.

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45

Thomas, Madhavi, Wei Dong Le, and Joseph Jankovic. "Minocycline and Other Tetracycline Derivatives: A Neuroprotective Strategy in Parkinson's Disease and Huntington's Disease." Clinical Neuropharmacology 26, no. 1 (January 2003): 18–23. http://dx.doi.org/10.1097/00002826-200301000-00005.

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46

Rubinsztein, David C., Jayne Leggo, Sandy Goodburn, David E. Barton, and Malcolm A. Ferguson-Smith. "Normal CAG and CCG repeats in the Huntington's disease genes of Parkinson's disease patients." American Journal of Medical Genetics 60, no. 2 (April 24, 1995): 109–10. http://dx.doi.org/10.1002/ajmg.1320600205.

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47

Cabarcas-Castro, L., J. Ramón-Gómez, A. Zarante-Bahamón, O. Bernal-Pacheco, E. Espinosa-García, and J. Cote-Orozco. "Westphal Variant of Huntington's Disease." Journal of Pediatric Neurology 17, no. 01 (November 13, 2017): 028–30. http://dx.doi.org/10.1055/s-0037-1608688.

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AbstractA Westphal variant of Huntington's disease (HD) is an infrequent presentation of this inherited neurodegenerative disorder. Here, we describe a 14-year-old girl who developed symptoms at the age of 7, with molecular evidence of abnormally expanded Cytosine-Adenine-Guanine (CAG) repeats in exon 1 of the Huntingtin gene. We briefly review the classical features of this variant highlighting the importance of suspecting HD in a child with parkinsonism and a family history of movement disorder or dementia.

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Davis, Laura, and Tom Dening. "Diagnostic, management and nursing challenges of less common dementias: Parkinsonian dementias and Huntington's disease." British Journal of Neuroscience Nursing 17, no. 2 (April 2, 2021): 68–76. http://dx.doi.org/10.12968/bjnn.2021.17.2.68.

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Background: Although most cases of dementia are caused by Alzheimer's disease or vascular dementia, around 10-15% of cases are due to other disorders, including dementias with Parkinsonian features, Huntington's disease, frontotemporal dementia, human immunodeficiency virus (HIV), and alcohol. Aims: These less common dementias are important as they may have differing clinical features and require different approaches to diagnosis and management. This paper seeks to provide relevant information for nurses about symptoms, diagnosis and management of some of the less common dementias. Methods: This is one of two connected papers, and provides a clinical overview of Parkinsonian dementias and Huntington's disease. It provides a narrative, rather than systematic, review of the literature. Findings: Parkinsonian dementias comprise Parkinson's disease dementia, dementia with Lewy bodies and so-called Parkinson's-plus syndromes (multi-system atrophy, progressive supranuclear palsy, and corticobasal degeneration). Huntington's disease is an inherited neuropsychiatric condition. Each has a distinctive clinical picture, with combinations of cognitive, neuropsychiatric and neurological symptoms but approaches to treatment and care are essentially supportive. Conclusions: Nurses have an essential role in supporting people with dementia, as well their families and carers, throughout the course of dementia from diagnosis to end of life care. They are often best placed and have the necessary skills to create appropriate care plans and to provide care management.

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McGeer, P. L., E. G. McGeer, S. Itagaki, and K. Mizukawa. "Anatomy and Pathology of the Basal Ganglia." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 14, S3 (August 1987): 363–72. http://dx.doi.org/10.1017/s0317167100037756.

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ABSTRACT:Neurotransmitters of the basal ganglia are of three types: I, amino acids; II, amines; and III, peptides. The amino acids generally act ionotropically while the amines and peptides generally act metabotropically. There are many examples of neurotransmitter coexistence in basal ganglia neurons. Diseases of the basal ganglia are characterized by selective neuronal degeneration. Lesions of the caudate, putamen, subthalamus and substantia nigra pars compacta occur, respectively, in chorea, dystonia, hemiballismus and parkinsonism. The differing signs and symptoms of these diseases constitute strong evidence of the functions of these various nuclei. Basal ganglia diseases can be of genetic origin, as in Huntington's chorea and Wilson's disease, of infectious origin as in Sydenham's chorea and postencephalitic parkinsonism, or of toxic origin as in MPTP poisoning. Regardless of the etiology, the pathogenesis is often regionally concentrated for reasons that are poorly understood. From studies on Parkinson and Huntington disease brains, evidence is presented that a common feature may be the expression of HLA-DR antigen on reactive microglia in the region where pathological neuronal dropout is occurring.

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Lindvall, Olle. "Neural Transplantation." Cell Transplantation 4, no. 4 (July 1995): 393–400. http://dx.doi.org/10.1177/096368979500400410.

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Cell transplantation is now being explored as a new therapeutic strategy to restore function in the diseased human central nervous system. Neural grafts show long-term survival and function in patients with Parkinson's disease but the symptomatic relief needs to be increased. Cell transplantation seems justified in patients with Huntington's disease and, at a later stage, possibly also in demyelinating disorders. The further development in this research field will require systematic studies in animal experiments but also well-designed clinical trials in small groups of patients.

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