Understanding the molecular basis of Parkinson’s disease, identification of biomarkers and routes to therapy

2010 ◽  
Vol 7 (4) ◽  
pp. 565-578 ◽  
Author(s):  
Philip A Robinson
2019 ◽  
Vol 94 ◽  
pp. 282-292 ◽  
Author(s):  
Luis C.S. Afonso ◽  
Gustavo H. Rosa ◽  
Clayton R. Pereira ◽  
Silke A.T. Weber ◽  
Christian Hook ◽  
...  

2002 ◽  
Vol 25 (5) ◽  
pp. 580-581
Author(s):  
Bernhard Bogerts

Dr. Northoff's comprehensive comparison of clinical symptoms and neurobiological findings in catatonia with that of Parkinson's disease through integration of various levels of investigation, from neurochemistry up to the subjective experience, is a good example of the new strategies we need to improve our understanding of psychiatric disorders. His multimodal approach, leading to the hypothesis that different pathophysiologies of transcortical “horizontal modulation” and “bottom-up/top-down” – orbitofrontal/basal ganglia – “vertical modulations,” may explain many clinical aspects of catatonia and Parkinson's disease, and thereby fills an important gap in current theories of psychomotor syndromes. However, to analyze more specifically the pathophysiology of catatonia, comparison not only with Parkinson's disease, but also with schizophrenia and anxiety disorders would be helpful. As long as the pathohistological and molecular basis of catatonic syndromes is unknown, theories based mainly on functional considerations remain preliminary.


2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Daniela M. Arduíno ◽  
A. Raquel Esteves ◽  
Sandra M. Cardoso

Understanding the molecular basis of Parkinson's disease (PD) has proven to be a major challenge in the field of neurodegenerative diseases. Although several hypotheses have been proposed to explain the molecular mechanisms underlying the pathogenesis of PD, a growing body of evidence has highlighted the role of mitochondrial dysfunction and the disruption of the mechanisms of mitochondrial dynamics in PD and other parkinsonian disorders. In this paper, we comment on the recent advances in how changes in the mitochondrial function and mitochondrial dynamics (fusion/fission, transport, and clearance) contribute to neurodegeneration, specifically focusing on PD. We also evaluate the current controversies in those issues and discuss the role of fusion/fission dynamics in the mitochondrial lifecycle and maintenance. We propose that cellular demise and neurodegeneration in PD are due to the interplay between mitochondrial dysfunction, mitochondrial trafficking disruption, and impaired autophagic clearance.


2012 ◽  
Vol 71 (3) ◽  
pp. 370-384 ◽  
Author(s):  
Nathan Pankratz ◽  
Gary W. Beecham ◽  
Anita L. DeStefano ◽  
Ted M. Dawson ◽  
Kimberly F. Doheny ◽  
...  

2018 ◽  
Vol 87 ◽  
pp. 67-77 ◽  
Author(s):  
Clayton R. Pereira ◽  
Danilo R. Pereira ◽  
Gustavo H. Rosa ◽  
Victor H.C. Albuquerque ◽  
Silke A.T. Weber ◽  
...  

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