Movement Disorders

Elias P. Casula, Isabella M. S. Mayer, Mahalekshmi Desikan, Sarah J. Tabrizi, John C. Rothwell, Michael Orth January 22, 2018

ABSTRACT

Background: In Huntington’s disease there is evidence of structural damage in the motor system, but it is still unclear how to link this to the behavioral disorder of movement. One feature of choreic movement is variable timing and coordination between sequences of actions.

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Wo-Tu Tian, Xiao-Jun Huang, Xiao Mao, Qing Liu, Xiao-Li Liu, Sheng Zeng, Xia-Nan Guo, Jun-Yi Shen, Yang-Qi Xu, Hui-Dong Tang, Xiao-Meng Yin, Mei Zhang, Wei-Guo Tang, Xiao-Rong Liu, Bei-Sha Tang, Sheng-Di Chen, Li Cao January 22, 2018

ABSTRACT

Background: Paroxysmal kinesigenic dyskinesia is the most common type of paroxysmal dyskinesia. Approximately half of the cases of paroxysmal kinesigenic dyskinesia worldwide are attributable to proline-rich transmembrane protein 2 mutations.

Objective: The objective of this study was to investigate potential causative genes and clinical characteristics in proline-rich transmembrane protein 2negative patients with paroxysmal kinesigenic dyskinesia.

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Caroline Tanner, Karen Marder, Shirley Eberly, Kevin Biglan, David Oakes, Ira Shoulson, January 16, 2018

ABSTRACT

Background

In Huntington’s disease, 60% of the variance in onset age is not explained by the huntingtin gene mutation. Huntington’s disease onset was earlier in caffeine users.

Objective

The objective of this study was to assess the relationship of lifestyle factors with motor phenoconversion among persons at risk for Huntington’s disease.

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Caroline Tanner, Karen Marder, Shirley Eberly, Kevin Biglan, David Oakes, Ira Shoulson, January 16, 2018

ABSTRACT

Background

In Huntington’s disease, 60% of the variance in onset age is not explained by the huntingtin gene mutation. Huntington’s disease onset was earlier in caffeine users.

Objective

The objective of this study was to assess the relationship of lifestyle factors with motor phenoconversion among persons at risk for Huntington’s disease.

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Elizabeth A. Coon, Jeremy K. Cutsforth-Gregory, Eduardo E. Benarroch January 16, 2018

Abstract

The synucleinopathies—Parkinson’s disease, dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure—result from distinct patterns of abnormal α-synuclein aggregation throughout the nervous system. Autonomic dysfunction in these disorders results from variable involvement of the central and peripheral autonomic networks.

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Elizabeth A. Coon, Jeremy K. Cutsforth-Gregory, Eduardo E. Benarroch January 16, 2018

Abstract

The synucleinopathies—Parkinson’s disease, dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure—result from distinct patterns of abnormal α-synuclein aggregation throughout the nervous system. Autonomic dysfunction in these disorders results from variable involvement of the central and peripheral autonomic networks.

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Yujing Gao, Gabrielle R. Wilson, Sarah E. M. Stephenson, Kiymet Bozaoglu, Matthew J. Farrer, Paul J. Lockhart January 16, 2018

ABSTRACT

The identification of pathogenic mutations in Ras analog in brain 39B (RAB39B) and Ras analog in brain 32 (RAB32) that cause Parkinson’s disease (PD) has highlighted the emerging role of protein trafficking in disease pathogenesis. Ras analog in brain (Rab) Guanosine triphosphatase (GTPase) function as master regulators of membrane trafficking, including vesicle formation, movement along cytoskeletal networks, and membrane fusion.

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Iris Y. Kim, Éilis J. O'Reilly, Katherine C. Hughes, Xiang Gao, Michael A. Schwarzschild, Marjorie L. McCullough, Marian T. Hannan, Rebecca A. Betensky, Alberto Ascherio January 16, 2018

ABSTRACT

Background: Caffeine intake has been inversely associated with Parkinson’s disease (PD) risk. This relationship may be modified by polymorphisms of glutamate ionotropic receptor NMDA type subunit 2A (GRIN2A) and cytochrome P450 1A2 (CYP1A2), but the results of previous studies have been inconsistent.

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