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Books on the topic 'Levy bodies'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

1944-, Perry R. H., McKeith I. G, Perry E. K, and International Workshop on Dementia with Lewy Bodies (1995 : Newcastle upon Tyne, England), eds. Dementia with Lewy bodies: Clinical, pathological, and treatment issues. Cambridge University Press, 1996.

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2

O'Brien, John. Dementia with Lewy bodies and Parkinson's disease dementia. Taylor & Francis, 2006.

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3

Parker, James N., and Philip M. Parker. The official patient's sourcebook on dementia with Lewy bodies. Edited by Icon Group International Inc and NetLibrary Inc. Icon Health Publications, 2002.

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4

Dementia with Lewy Bodies: Clinical, Pathological, and Treatment Issues. Cambridge University Press, 1996.

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5

Githire, Njeri. Immigration, Assimilation, and Conflict. University of Illinois Press, 2017. http://dx.doi.org/10.5406/illinois/9780252038785.003.0003.

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This chapter examines the deployment of counter-incorporative strategies as a means to thwart potentially dangerous elements from entering the eating body. In particular, it examines how, through the language of disease and contamination that proliferates in the realm of immigration and its effect on culture, select national cultures are portrayed as under attack from foreigners and their filthy, debased bodies. Marked with cannibalism as the ultimate expression of savagery and human degradation, these bodies evoke anxiety and deep-seated fear of extinction in the national consciousness. Focus

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6

Rongve, Arvid, and Dag Aarsland. Dementia with Lewy bodies and Parkinson’s disease dementia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0035.

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Dementia with Lewy bodies and Parkinson’s disease dementia belong to the α-synucleinopathies, a family of diseases pathologically characterized by aggregation of α-synuclein in Lewy bodies in the brain. In this chapter we present the epidemiological data for both conditions including new data on MCI. Clinical diagnostic criteria are reviewed and the different neuropathology staging systems for DLB and PDD and the most important genetic findings are considered. Biomarkers in DLB and PDD with particular focus on imaging techniques like CIT-SPECT and MRI are described. Important clinical symptoms

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7

Szczeszak-Brewer, Agata. Sex and Nation in Transatlantic Literatures. Bloomsbury Publishing Plc, 2025. https://doi.org/10.5040/9781350323360.

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Nationalist and tribal cohesion in Ireland, South Africa, the US, and elsewhere often relies on an absence of female and gender-nonconforming bodies in the public life. Staging a vital counter-narrative to global nationalist discourses, this book explores how 20th and 21st-century postcolonial literatures criticize hetero-normative definitions of nationhood across different geopolitical and cultural contexts. Szczeszak-Brewer delves into the metaphorical currency of male impotence and sexual aggression in nationalist narratives. She examines the place of gender-nonconforming characters in lite

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8

O'Brien, John. Dementia with lewy bodies and Parkinson's disease dementia /$bedited by John O'Brien ... [et al.]. 2006.

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9

Fox, Susan H., and Marina Picillo. “I See Them Sitting on My Bed, Doctor”. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0012.

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Many movement disorders specialists would consider dementia with Lewy bodies to be on one end of a spectrum of presentations associated with Lewy body pathology. Parkinson’s disease with preserved cognition sits at the other end of the spectrum, and over time it can be associated with a greater cortical Lewy body burden and related cognitive impairment. It is unclear what determines to what degree cognitive impairment is involved in a given patient, and the arbitrary time-based division between Parkinson’s disease and dementia with Lewy bodies is imperfect, although it serves to help recogniti

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10

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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11

Kolvin, Philip. Licensed Premises. 2nd ed. Bloomsbury Professional Ltd, 2020. http://dx.doi.org/10.5040/9781526519382.

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Licensed Premises: Law, Practice and Policy, Second Edition is a highly practical guide to the licensed industry. It clearly explains, through the use of case studies, practical tools and strategic policy advice, how the licensing regime, allied to other statutory and voluntary schemes, can be used to develop a more sustainable, diverse leisure economy. Untangling the web of licensing law: The second edition is supported by copious charts and tables to simplify explanations and argues for a strategic approach to licensing, explaining how it is part of a much larger web of control of the night

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12

Carton, James. Neuropathology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199591633.003.0017.

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Nervous system malformations 322Epilepsy 323Head injury 324Cerebral infarction 325Intracerebral haemorrhage 326Subarachnoid haemorrhage 328Meningitis 330Cerebral infections 331Multiple sclerosis 332Alzheimer's disease 333Dementia with Lewy bodies 334Parkinson's disease 335Huntington's disease 336Motor neurone disease 337Creutzfeldt–Jacob disease ...

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13

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Dementia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0011.

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This chapter discusses the clinical features and evidence-based pharmacological management of dementia disorders (Alzheimer’s disease (AD), vascular dementia, dementia with Lewy bodies (DLB), Parkinson’s disease dementia (PDD), frontotemporal dementia (FTD), mixed dementia, and mild cognitive impairment (MCI)).

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14

Ahlskog, J. Eric. Dementia with Lewy Bodies and Parkinson's Disease Dementia: Patient, Family, and Clinician Working Together for Better Outcomes. Oxford University Press, Incorporated, 2013.

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15

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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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

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16

Kaplan, Tamara, and Tracey Milligan. Movement Disorders 2: Parkinson’s Plus and Degenerative Diseases (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0012.

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The video in this chapter explores movement disorders, and focuses on Parkinson’s Plus and degenerative diseases. It outlines the features and pathology of dementia with lewy bodies (DLB), progressive supranuclear palsy (PSP), multiple systems atrophy (MSA) and corticobasal degeneration (CBD), as well as genetic movement disorders, Wilson’s disease, and Huntington’s disease.

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17

Pillai, Jagan A., and James B. Leverenz. Pathogenesis of Lewy Body Dementia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0020.

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This chapter discusses the Pathogenesis of Lew Body Dementia. The Lewy body dementias (LBDs) are a spectrum of dementing neurodegenerative disorders underpinned by the pathological accumulation of α- synuclein protein in both intraneuronal inclusions, “Lewy bodies, ” and neuronal processes, “Lewy neurites”. The chapter concludes that, as with other forms of cognitive impairment in the aged, the pathophysiology of cognitive impairment in LBD is likely multifactorial. Although it appears that α- synuclein pathology, particularly in the limbic and neocortical regions are linked to cognitive chang

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18

Carton, James. Neuropathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0018.

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This chapter discusses neuropathology, including nervous system malformations, epilepsy, head injury, cerebral infarction, intracerebral haemorrhage, subarachnoid haemorrhage, meningitis, cerebral infections, multiple sclerosis, Guillain–Barré syndrome, myasthenia gravis, Alzheimer’s disease, vascular dementia, dementia with Lewy bodies, Parkinson’s disease, Huntington’s disease, motor neurone disease, Creutzfeldt–Jacob disease, astrocytomas (including glioblastoma), oligodendroglioma, ependymoma, meningioma, medulloblastoma, primary CNS lymphomas, and cerebral metastases.

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19

Ahlskog, J. Eric. Dementia with Lewy Body and Parkinson's Disease Patients. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780199977567.001.0001.

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Patients, spouses, families, and caregivers dealing with dementia face a host of complex issues, particularly when they must confront Dementia with Lewy Bodies or Parkinson's Disease. Until now there has been no guidebook for the general public to help navigate these challenging disorders. In Dementia with Lewy Bodies and Parkinson's Disease Dementia, Dr. J. Eric Ahlskog draws on 30 years of clinical and research work at Mayo Clinic to arm patients and families with crucial information that will enable them to work in tandem with their doctors. A diagnosis of dementia can be devastating, leavi

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20

Piggott, Margaret Ann. Neurochemical pathology of dementia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0007.

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This chapter considers the neurodegenerative disorders Alzheimer’s disease (AD), Lewy body dementias (dementia with Lewy bodies (DLB) and Parkinson’s disease dementia(PDD)), frontotemporal dementia (FTD); and also vascular dementia (VaD) which results from cerebrovascular disease. These different conditions, which give rise to dementia syndromes, each have distinct neurochemical pathologies, with important implications for treatment. As increased age is the common risk factor generally associated with dementing illnesses, neurochemical changes are set in the context of the changes which occur

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21

Fox, Susan H., and Marina Picillo. Becoming a Little Forgetful. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0003.

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Many patients with Parkinson’s disease will experience some degree of cognitive impairment during the course of their disease. Cortical involvement in the underlying synuclein pathology is variable in its severity and extent. The most severe end of the spectrum is seen in dementia with Lewy bodies, in which cognitive impairment is prominent from the beginning. In most patients, however, mild memory difficulty and executive dysfunction are present to some degree but do not impair function until the later stages of the disease; after 20 years, dementia is almost universal and can be as disabling

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22

Hodges, John R. Delirium and Dementia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198749189.003.0002.

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Delirium and dementia affect one or more cognitive domains with a distributed neural basis—attention, memory, and executive function—in some instances accompanied by more focal cognitive deficits. Patients with one, or both, of these conditions constitute the commonest presentation in behavioural neurology and in geriatric psychiatry. This chapter first describes the core characteristics and causes of delirium. This is followed by a description of the major causes of dementia notably, Alzheimer’s disease, frontotemporal dementia, Huntington’s disease, dementia with Lewy bodies, and progressive

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23

Bekris, Lynn M., and James B. Leverenz. Genetics of Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0010.

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A great deal has been discovered about Neurodegenerative disorders (NDDs) including Alzheimer’s disease, Parkinson’s disease, frontotemporal dementia, dementia with Lewy bodies . This includes genetic variants associated with both sporadic and autosomal dominant NDDs. These findings have been crucial in our understanding the underlying factors that drive neuropathological changes and in clarifying the time line of biomarker changes in presymptomatic autosomal dominant mutation carriers. While much is still to be learned, these findings will play an important role in the future of neurodegenera

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24

Manni, Raffaele, and Michele Terzaghi. Sleep disorders in neurodegenerative diseases other than Parkinson disease and multiple system atrophy. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0026.

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This chapter examines sleep–wake disturbances occurring in the most common neurodegenerative disorders. It reviews sleep alterations in Alzheimer disease and dementia with Lewy bodies. It also discusses sleep problems in progressive supranuclear palsy, corticobasal degeneration, Huntington disease, and spinocerebellar ataxias. Status dissociatus as an extreme form of sleep alteration in advanced neurodegenerative diseases is also considered. The chapter reviews the key points for the treatment of disrupted sleep in neurodegenerative disorders, with a focus on pharmacological and nonpharmacolog

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25

Padilla, Claudia R., and Mario F. Mendez. Neuropsychiatric Features Across Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0006.

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Neuropsychiatric symptoms (NPS) are a major manifestation of neurodegenerative diseases(NDDs) including Alzheimer’s disease (AD), Dementia with Lewy Bodies (DLB) and frontotemporal dementia (FTD). NPS symptoms are a determining factor impacting economic and psychological costs for both the patient and their caregivers in these devastating illness. Recent developments in neuroscience have clarified the relationship of NPS with changes in brain structures, alterations in neural circuits and networks, and their neurotransmitter systems. It is increasingly recognized that NPS shared across differe

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26

Tousi, Babak. Cognitive Enhancement in Non-Alzheimer’s Dementias. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190214401.003.0004.

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Cognitive enhancement in non-Alzheimer’s dementias has not been studied as extensively as that in Alzheimer’s dementia. This chapter reviews the research on cognitive enhancement for three types of dementia: vascular dementia, dementia with Lewy bodies, and frontal lobe dementia. The chapter reviews both pharmacological and nonpharmacological approaches for treatment of dementia. The focus is on randomized controlled trials for currently available medications, specifically cholinesterase inhibitors and memantine. Major advances in physical and cognitive rehabilitation during the past decade ha

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27

North, Dan, Bob Rehak, and Michael S. Duffy, eds. Special Effects. 2nd ed. Palgrave, 2015. https://doi.org/10.5040/9781838711283.

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As blockbusters employ ever greater numbers of dazzling visual effects and digital illusions, this book explores the material roots and stylistic practices of special effects and their makers. Gathering leading voices in cinema and new media studies, this comprehensive anthology moves beyond questions of spectacle to examine special effects from the earliest years of cinema, via experimental film and the Golden Age of Hollywood, to our contemporary transmedia landscape. Wide-ranging and accessible, this book illuminates and interrogates the vast array of techniques film has used throughout its

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28

O’Brien, John T., and Louise Grayson. Mild Cognitive Impairment and predementia syndromes. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0032.

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Mild cognitive impairment is a term used to describe a condition or conditions where subjects have recognisable degrees of objective cognitive impairment which fall short of current standardised definitions for either a dementia syndrome in general, or for particular disorders such as Alzheimer’s disease, dementia with Lewy bodies or frontotemporal dementia. This chapter summarises some of the key issues surrounding the historical development of pre-dementia syndromes, considers the conceptual issues related to the use of the term mild cognitive impairment as a diagnosis, summarises what is kn

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29

Deramecourt, Vincent, Florence Lebert, and Florence Pasquier. Frontotemporal dementia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0036.

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Frontotemporal dementia (FTD) is the second most common form of dementia in persons younger than 65 years after Alzheimer’s disease. The FTD spectrum is characterized by clinical, molecular and genetic heterogeneity. Core features of FTD are behavioural and language manifestations and the clinical spectrum of FTD currently includes a behavioural variant, progressive nonfluent aphasia and semantic dementia. The most common behavioural features are disinhibition, apathy, loss of empathy, hyperorality and perseveration. Neuroimaging usually demonstrates focal atrophy and hypometabolism in the ant

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30

Walsh, Richard A., Robertus M. A. de Bie, and Susan H. Fox, eds. Movement Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.001.0001.

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Part of the “What Do I Do Now?” series, Movement Disorders uses a case-based approach to cover common and important topics in the examination, investigation, and management of Parkinson’s disease, gait disorders, dystonia, and other movement disorders. Each chapter provides a discussion of the diagnosis, key points to remember, and selected references for further reading. For this edition, all cases and references have been updated and 15 new cases have been added, including the following: genetic testing in Parkinson’s disease, dementia with Lewy bodies, fragile X tremor ataxia syndrome, use

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31

Kelly, Thomas J., and Mijail Serruya. Integrative Approaches to Cognitive Decline. Edited by Anthony J. Bazzan and Daniel A. Monti. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190690557.003.0017.

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The ability to remember, plan, communicate, and multitask changes with normal, healthy aging. These cognitive abilities decline more rapidly and with greater severity in the setting of neurodegenerative disease. The most common etiology of neurodegenerative cognitive decline is Alzheimer’s disease, and other processes, such as those triggered by stroke, dementia with Lewy bodies, and traumatic brain injury, also cause significant debility. The purpose of this chapter is to review evidence-based integrative medical interventions that may slow both normal and disease-related cognitive decline in

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32

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 o

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33

Attems, Johannes, and Kurt A. Jellinger. Neuropathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0006.

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This chapter describes the main neuropathological features of the most common age associated neurodegenerative diseases including Alzheimer's disease, Parkinson's disease and dementia with Lewy bodies as well as other less frequent ones such as multiple system atrophy, Pick's disease, corticobasal degeneration, progressive supranuclear palsy, argyrophilic grain disease, neurofibrillary tangle dominant dementia, frontotemporal lobar degeneration with TDP-43 pathology and Huntington's disease. Likewise cerebral amyloid angiopathy, hippocampal sclerosis, vascular dementia and prion diseases are d

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34

McBurney, John W. Pesticides and Neurodegenerative Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190490911.003.0008.

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Neurodegenerative diseases, which are characterized by neuronal degeneration, include Alzheimer disease (AD), Parkinson disease (PD), and amyotrophic lateral sclerosis (ALS). Their worldwide prevalence is increasing as the global population ages. The causes reflect interactions between genetics and environmental factors such as increasing urbanization, industrialization, and widespread use of chemicals, including insecticides, fungicides, and herbicides. Epidemiologic data suggest that exposure to many of these pesticides increases the risk of neurodegeneration. The best-defined mechanism for

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35

Postuma, Ronald B. REM sleep behavior disorder. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0038.

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A diagnosis of REM sleep behavior disorder (RBD), a disorder characterized by “acting out” of dreams during REM sleep, has critical implications for a patient’s future. Aside from being a treatable parasomnia, usually managed with melatonin or clonazepam, RBD is the most powerful risk factor for Parkinson disease and dementia with Lewy bodies yet discovered. Over 70% of patients with idiopathic RBD will develop a neurodegenerative synucleinopathy. Moreover, the disease course is more severe in patients with RBD than those without. Numerous screens have been developed to aid detection, and clin

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36

Rossor, Martin. Neuropsychological disorders, dementia, and behavioural neurology. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0755.

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The diseases which disrupt the cerebral cortex and its subcortical connections result in a wide variety of clinical features. These include the classical syndromes of higher cortical dysfunction such as the dysphasias, dyspraxias, amnesias, and agnosias together with a wide variety of behavioural and emotional disturbances. Such disorders frequently overlap with the clinical disciplines of clinical psychology and psychiatry. Historically there has been a broad split between those diseases which are seen by neurologists and those that are seen by psychiatrists. To some extent the distinction re

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