1
40
2
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.bbr.2018.01.029" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bbr.2018.01.029</a>
Pages
41–49
Volume
343
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Exacerbation of sensorimotor dysfunction in mice deficient in Atp13a2 and overexpressing human wildtype alpha-synuclein.
Publisher
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Behavioural brain research
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-05
Subject
The topic of the resource
*Alpha-synuclein; *ATP13A2; *Mice; *Phenotype; *Sensorimotor; Adenosine Triphosphatases/*deficiency/genetics; alpha-Synuclein/genetics/*metabolism; Animal; Animals; Body Temperature; Body Weight; Disease Models; Female; Gait Disorders; Humans; Inbred C57BL; Male; Membrane Proteins/*deficiency/genetics; Mice; Motor Skills/physiology; Neurologic/*metabolism; Phenotype; Severity of Illness Index; Sex Characteristics; Transgenic
Creator
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Dirr Emily R; Ekhator Osunde R; Blackwood Rachel; Holden John G; Masliah Eliezer; Schultheis Patrick J; Fleming Sheila M
Description
An account of the resource
Loss of function mutations in the gene ATP13A2 are associated with Kufor-Rakeb Syndrome and Neuronal Ceroid Lipofuscinosis, the former designated as an inherited form of Parkinson's disease (PD). The function of ATP13A2 is unclear but in vitro studies indicate it is a lysosomal protein and may interact with the presynaptic protein alpha-synuclein (aSyn) and certain heavy metals. Accumulation of aSyn is a major component of lewy bodies, the pathological hallmark of PD. Atp13a2-deficient (13a2) mice develop age-dependent sensorimotor deficits, and accumulation of insoluble aSyn in the brain. To better understand the interaction between ATP13A2 and aSyn, double mutant mice with loss of Atp13a2 function combined with overexpression of human wildtype aSyn were generated. Female and male wildtype (WT), 13a2, aSyn, and 13a2-aSyn mice were tested on a battery of sensorimotor tests including adhesive removal, challenging beam traversal, spontaneous activity, gait, locomotor activity, and nest-building at 2, 4, and 6 months of age. Double mutant mice showed an earlier onset and accelerated alterations in sensorimotor function that were age, sex and test-dependent. Female 13a2-aSyn mice showed early and progressive dysfunction on the beam and in locomotor activity. In males, 13a2-aSyn mice showed more severe impairments in spontaneous activity and adhesive removal. Sex differences were also observed in aSyn and 13a2-aSyn mice on the beam, cylinder, and adhesive removal tests. In other tasks, double mutant mice displayed deficits similar to aSyn mice. These results indicate loss of Atp13a2 function exacerbates the sensorimotor phenotype in aSyn mice in an age and sex-dependent manner.
Identifier
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<a href="http://doi.org/10.1016/j.bbr.2018.01.029" target="_blank" rel="noreferrer noopener">10.1016/j.bbr.2018.01.029</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Alpha-synuclein
*ATP13A2
*Mice
*Phenotype
*Sensorimotor
2018
Adenosine Triphosphatases/*deficiency/genetics
alpha-Synuclein/genetics/*metabolism
Animal
Animals
Behavioural brain research
Blackwood Rachel
Body Temperature
Body Weight
Department of Pharmaceutical Sciences
Dirr Emily R
Disease Models
Ekhator Osunde R
Female
Fleming Sheila M
Gait Disorders
Holden John G
Humans
Inbred C57BL
Male
Masliah Eliezer
Membrane Proteins/*deficiency/genetics
Mice
Motor Skills/physiology
NEOMED College of Pharmacy
Neurologic/*metabolism
Phenotype
Schultheis Patrick J
Severity of Illness Index
Sex Characteristics
Transgenic
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s40572-017-0143-2" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s40572-017-0143-2</a>
Pages
192–199
Issue
2
Volume
4
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Mechanisms of Gene-Environment Interactions in Parkinson's Disease.
Publisher
An entity responsible for making the resource available
Current environmental health reports
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-06
Subject
The topic of the resource
*Alpha-synuclein; *ATP13A2; *Gene-Environment Interaction; *Genetic Predisposition to Disease; *Manganese; *Paraquat; *Parkinson Disease; *Parkinson's disease; *Rotenone; Environmental Exposure/*adverse effects; Herbicides/adverse effects; Humans; Insecticides/adverse effects; Mutation/genetics; Paraquat/adverse effects; Risk Factors; Rotenone/adverse effects
Creator
An entity primarily responsible for making the resource
Fleming Sheila M
Description
An account of the resource
PURPOSE OF REVIEW: The purpose of the study was to discuss the main mechanisms associated with environmental and genetic factors that contribute to the development of Parkinson's disease (PD). RECENT FINDINGS: Novel genetic contributors to PD are being identified at a rapid pace in addition to novel environmental factors. The discovery of mutations in alpha-synuclein and leucine-rich repeat kinase 2 causing inherited forms of PD along with epidemiological, in vitro, and in vivo studies identifying herbicides, pesticides, and metals as risk factors have dramatically improved our understanding of mechanisms involved in the development of PD. However, at the same time, these discoveries have also added layers of complexity to the disease. Within the last several years, the genetics associated with PD has dominated the field in many ways; however, the majority of PD cases are likely due to different combinations of environmental exposures and genetic susceptibility. The most common toxicants used to model PD including rotenone, paraquat, and
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s40572-017-0143-2" target="_blank" rel="noreferrer noopener">10.1007/s40572-017-0143-2</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Alpha-synuclein
*ATP13A2
*Gene-Environment Interaction
*Genetic Predisposition to Disease
*Manganese
*Paraquat
*Parkinson Disease
*Parkinson's disease
*Rotenone
2017
Current environmental health reports
Department of Pharmaceutical Sciences
Environmental Exposure/*adverse effects
Fleming Sheila M
Herbicides/adverse effects
Humans
Insecticides/adverse effects
Mutation/genetics
NEOMED College of Pharmacy
Paraquat/adverse effects
Risk Factors
Rotenone/adverse effects