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Books on the topic 'Alpha synuclein'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 December 2024

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1

Bartels, Tim, ed. Alpha-Synuclein. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9124-2.

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2

Mente, Peter. Alteration in the metabolism of [alpha]-synuclein leads to aggregate formation in dementia with lewy bodies. Ottawa: National Library of Canada, 2003.

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3

Bartels, Tim. Alpha-Synuclein: Methods and Protocols. Springer New York, 2019.

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4

Schiesser, William E. ODE/PDE α-Synuclein Models for Parkinson's Disease. Elsevier Science & Technology Books, 2018.

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5

Schiesser, William E. ODE / PDE Alpha-Synuclein Models for Parkinson's Disease. Elsevier Science & Technology Books, 2018.

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6

Luth, Eric. Physiological and Pathological Characterization of Alpha-Synuclein Oligomers. 2014.

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7

Kontopoulos, Eirene. Mechanisms of alpha-synuclein neurotoxicity in Parkinson's disease. 2007.

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8

Xu, Pingyi, Shaomin Li, Liu Jun, Yun-Cheng Wu, Shaogang Qu, and Hao Deng, eds. Biomarkers and Pathogenesis of Alpha-Synuclein in Parkinson's Disease. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-143-4.

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9

Polizzi, Mark, and Howard C. Kanowitz. Alpha-Synuclein: Functional Mechanisms, Structure & Role in Parkinson's Disease. Nova Science Publishers, Incorporated, 2013.

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10

Rappley, Irit. Selective effects of alpha-synuclein on membrane phospholipids and mitochondrial function. 2009.

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11

Manfredsson, Fredric P., Ruth G. Perez, and Ivette Martinez Sandoval, eds. The Protein Alpha-Synuclein: Its Normal Role (in Neurons) and its Role in Disease. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-610-5.

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12

Galvin, James E., and Jose Tomas Bras. Neurobiology of Lewy Body Dementias. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0055.

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Abstract:

Lewy body dementia (LBD) is the second most common form of neurocognitive disorder after Alzheimer’s disease and covers two related diagnoses: Dementia with Lewy Bodies and Parkinson’s Disease Dementia. Despite being a common disorder, diagnosis outside expert academic centers remains a significant challenge. The core pathological feature of LBD is the cortical Lewy body; however, many cases will have coexistent Alzheimer disease pathology. Genetic risk factors for LBD include mutations in genes for alpha-synuclein (SNCA) and galactocerbrosidase (GBA). Dopamine transporter imaging remains the most sensitive but platforms for measuring alpha-synuclein are being developed. Current therapies focus on symptomatic relief but experimental cell and animal models are providing new insights for the development of disease-modifying therapeutics.

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13

Soileau, Michael J., and Kelvin L. Chou. Parkinson Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0002.

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Parkinson disease is a neurodegenerative disorder characterized clinically by tremor, rigidity, bradykinesia, and postural instability and pathologically by loss of nigrostriatal neurons and deposition of alpha-synuclein in neuronal cell bodies and neuritis. Non-motor symptoms such as psychiatric disorders, cognitive abnormalities, sleep dysfunction, autonomic dysfunction, and sensory manifestations are also common. This chapter gives a broad overview of this disorder. Sections cover pathophysiology, genetics, clinical manifestations, and disease course. The chapter also briefly discusses how to make the diagnosis, and alternative conditions that should be considered.

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14

Turk, Bela R., and Ali Fatemi. Diagnosis and Therapy for Lewy Body Dementia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0019.

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Almost undistinguished some 30 years ago, dementia with Lewy bodies is now shown to be the second most common neurodegenerative cause of dementia in the elderly. A host of neuroinflammatory mechanisms are attributed to Lewy bodies and their component alpha synuclein, a common pathology shared by Parkinson disease and Parkinson disease with dementia. Accurate diagnosis of patients is essential, as they show unique impairment patterns, which differ from other forms of dementia and show severe adverse reaction to neuroleptic medication, a common treatment in other degenerative diseases.

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15

Lees, A. J. Parkinson’s disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0008.

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The following landmark discoveries in our understanding of Parkinson’s disease are considered in this chapter: the first full medical description of the malady; consistent severe loss of pigmented cells in the substantia nigra; severe depletion of striatal dopamine; the use of high doses of racemic dopa to improve the motor symptoms; a superior animal model for the study of potential new treatments; functional lesioning and deep brain stimulation to relieve symptoms; capability of fetal dopamine cells to reinnervate the striatum and improve handicap; a compensatory phase before the emergence of motor symptoms and nigral cell loss beginning about five years prior to the onset of presenting symptoms; a large autosomal dominant family with Parkinsonism found to carry a genetic mutation of alpha synuclein; and discovery of Lewy bodies in surviving grafted fetal neuronal cells many years after successful implantation.

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16

Démence à Corps de Lewy: Béta-Amyloïde et Alpha-synucléine. Independently Published, 2021.

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