The road less traveled: Alternative pathways for action-verb processing in Parkinson’s disease

2016 ◽  
Vol 108 ◽  
pp. 114-115 ◽  
Author(s):  
Sofía Abrevalla ◽  
Lucas Sedeno ◽  
Sol Fitipaldi ◽  
Agustin Ibañez ◽  
Adolfo García-Cordero
2016 ◽  
Vol 55 (4) ◽  
pp. 1429-1435 ◽  
Author(s):  
Sofía Abrevaya ◽  
Lucas Sedeño ◽  
Sol Fitipaldi ◽  
David Pineda ◽  
Francisco Lopera ◽  
...  

2013 ◽  
Vol 218 (6) ◽  
pp. 1355-1373 ◽  
Author(s):  
Juan Felipe Cardona ◽  
Oscar Gershanik ◽  
Carlos Gelormini-Lezama ◽  
Alexander Lee Houck ◽  
Sebastian Cardona ◽  
...  

2015 ◽  
Vol 137 (4) ◽  
pp. 2431-2432
Author(s):  
Emily Wang ◽  
Lee K. Walters ◽  
Leo A. Verhagen Metman

2014 ◽  
Vol 5 (2) ◽  
Author(s):  
Adolfo García ◽  
Agustín Ibáñez

AbstractA growing body of evidence indicates that neurodegenerative motor disorders involved high-order cognitive dysfunctions. Crucially, evidence obtained in multiple behavioral, neuroimaging, and electrophysiological studies points to selective impairments of action language -that is, processing of linguistic stimuli denoting motor actions, including idioms (e.g., cut a rug) and action verbs (e.g., clap). Action-verb deficits (with relative preservation of noun processing) have been repeatedly documented in Parkinson’s disease (PD). However, research on relevant biomarkers is still scant, and clinical implications of these findings have not yet been formally discussed. Relevant insights may be obtained through the assessment of motor-language coupling (i.e., the behavioral and neural integration of action-verb processing and ongoing motor actions). We propose that motorlanguage coupling deficits, as indexed by a cortical-subcortical network, may constitute an early neurocognitive marker of PD. Specifically, deficits in this domain at the prodromal stage may be detected through the actionsentence compatibility (ACE) paradigm, which induces a contextual coupling of ongoing motor actions and action-verb processing. Our translational proposal is supported and illustrated by recent studies demonstrating the sensitivity of the ACE technique as well as its potential to assist in differential diagnosis and interventionprogram design.


Cortex ◽  
2009 ◽  
Vol 45 (8) ◽  
pp. 960-971 ◽  
Author(s):  
Patrice Péran ◽  
Dominique Cardebat ◽  
Andrea Cherubini ◽  
Fabrizio Piras ◽  
Giacomo Luccichenti ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-20 ◽  
Author(s):  
A. R. Esteves ◽  
D. M. Arduíno ◽  
D. F. F. Silva ◽  
C. R. Oliveira ◽  
S. M. Cardoso

While the etiology of Parkinson's disease remains largely elusive, there is accumulating evidence suggesting that mitochondrial dysfunction occurs prior to the onset of symptoms in Parkinson's disease. Mitochondria are remarkably primed to play a vital role in neuronal cell survival since they are key regulators of energy metabolism (as ATP producers), of intracellular calcium homeostasis, of NAD+/NADH ratio, and of endogenous reactive oxygen species production and programmed cell death. In this paper, we focus on mitochondrial dysfunction-mediated alpha-synuclein aggregation. We highlight some of the findings that provide proof of evidence for a mitochondrial metabolism control in Parkinson's disease, namely, mitochondrial regulation of microtubule-dependent cellular traffic and autophagic lysosomal pathway. The knowledge that microtubule alterations may lead to autophagic deficiency and may compromise the cellular degradation mechanisms that culminate in the progressive accumulation of aberrant protein aggregates shields new insights to the way we address Parkinson's disease. In line with this knowledge, an innovative window for new therapeutic strategies aimed to restore microtubule network may be unlocked.


2022 ◽  
Vol 61 ◽  
pp. 101040
Author(s):  
Edoardo Nicolò Aiello ◽  
Margherita Grosso ◽  
Asia Di Liberto ◽  
Adele Andriulo ◽  
Simona Buscone ◽  
...  

2009 ◽  
Vol 61 (6) ◽  
pp. 966-977 ◽  
Author(s):  
Bessy Thrash ◽  
Kariharan Thiruchelvan ◽  
Manuj Ahuja ◽  
Vishnu Suppiramaniam ◽  
Muralikrishnan Dhanasekaran

Sign in / Sign up

Export Citation Format

Share Document