scholarly journals Disclosure of research results in genetic studies of Parkinson's disease caused by LRRK2 mutations

2015 ◽  
Vol 30 (7) ◽  
pp. 904-908 ◽  
Author(s):  
Claustre Pont-Sunyer ◽  
Susan Bressman ◽  
Deborah Raymond ◽  
Amanda Glickman ◽  
Eduardo Tolosa ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Genetic Studies ◽  
Research Results

Genetic studies in Parkinson's disease with an α-synuclein/NACP gene polymorphism in Japan

2001 ◽  
Vol 300 (2) ◽  
pp. 125-127 ◽  
Author(s):  
Yuishin Izumi ◽  
Hiroyuki Morino ◽  
Masaya Oda ◽  
Hirofumi Maruyama ◽  
Fukashi Udaka ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Gene Polymorphism ◽  
Genetic Studies

scholarly journals Historical and cross-cultural perspectives on Parkinson’s disease

2018 ◽  
Vol 15 (3) ◽  
Author(s):  
Lee Xenakis Blonder
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Disorder ◽  
Ancient Greek ◽  
Genetic Studies ◽  
Cultural Perspectives ◽  
Paralysis Agitans ◽  
Ancient Times ◽  
Jean Martin Charcot ◽  
British Physician

Abstract Parkinson’s disease (PD) is a common neurodegenerative disorder, affecting up to 10 million people worldwide according to the Parkinson’s Disease Foundation. Epidemiological and genetic studies show a preponderance of idiopathic cases and a subset linked to genetic polymorphisms of a familial nature. Traditional Chinese medicine and Ayurveda recognized and treated the illness that Western Medicine terms PD millennia ago, and descriptions of Parkinson’s symptomatology by Europeans date back 2000 years to the ancient Greek physician Galen. However, the Western nosological classification now referred to in English as “Parkinson’s disease” and the description of symptoms that define it, are accredited to British physician James Parkinson, who in 1817 authored The Shaking Palsy. Later in the nineteenth century, French neurologist Jean-Martin Charcot re-labeled paralysis agitans “Parkinson’s disease” and over a century of scientific research ensued. This review discusses European, North American, and Asian contributions to the understanding and treatment of PD from ancient times through the twentieth century.

scholarly journals Inflammatory bowel disease and Parkinson’s disease: common pathophysiological links

Gut ◽  
2020 ◽  
pp. gutjnl-2020-322429 ◽  
Author(s):  
Ho-Su Lee ◽  
Evy Lobbestael ◽  
Séverine Vermeire ◽  
João Sabino ◽  
Isabelle Cleynen
Keyword(s):  
Parkinson’S Disease ◽  
Inflammatory Bowel Disease ◽  
Parkinson's Disease ◽  
Bowel Disease ◽  
Population Based ◽  
Leucine Rich Repeat ◽  
Causal Gene ◽  
Genetic Studies ◽  
Inflammatory Bowel ◽  
Shared Genetic

Inflammatory bowel disease and Parkinson’s disease are chronic progressive disorders that mainly affect different organs: the gut and brain, respectively. Accumulating evidence has suggested a bidirectional link between gastrointestinal inflammation and neurodegeneration, in accordance with the concept of the ‘gut–brain axis’. Moreover, recent population-based studies have shown that inflammatory bowel disease might increase the risk of Parkinson's disease. Although the precise mechanisms underlying gut–brain interactions remain elusive, some of the latest findings have begun to explain the link. Several genetic loci are shared between both disorders with a similar direction of effect on the risk of both diseases. The most interesting example is LRRK2 (leucine-rich repeat kinase 2), initially identified as a causal gene in Parkinson's disease, and recently also implicated in Crohn’s disease. In this review, we highlight recent findings on the link between these seemingly unrelated diseases with shared genetic susceptibility. We discuss supporting and conflicting data obtained from epidemiological and genetic studies along with remaining questions and concerns. In addition, we discuss possible biological links including the gut–brain axis, microbiota, autoimmunity, mitochondrial function and autophagy.

Danish—American family (family E) with ‘Parkinson's Disease’: Pitfalls of genetic studies

1996 ◽  
Vol 2 (1) ◽  
pp. 47-49 ◽  
Author(s):  
Zbigniew K. Wszolek ◽  
Ronald F. Peeiffer ◽  
Melody A. Denson ◽  
Rodney D. McComb
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
American Family ◽  
Genetic Studies

scholarly journals Human-genome gut-microbiome interaction in Parkinson’s disease

2021 ◽  
Author(s):  
Zachary D. Wallen ◽  
William J. Stone ◽  
Stewart A. Factor ◽  
Eric Molho ◽  
Cyrus P. Zabetian ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Human Genome ◽  
Gut Microbiome ◽  
Alpha Synuclein ◽  
Susceptibility Loci ◽  
Opportunistic Pathogens ◽  
Host Genotype ◽  
Genetic Studies ◽  
Genome Wide

AbstractThe causes of complex diseases remain an enigma despite decades of epidemiologic research on environmental risks and genome-wide studies that have uncovered tens or hundreds of susceptibility loci for each disease. We hypothesize that the microbiome is the missing link. Genetic studies have shown that overexpression of alpha-synuclein, a key pathological protein in Parkinson’s disease (PD), can cause familial PD and variants at alpha-synuclein locus confer risk of idiopathic PD. Recently, dysbiosis of gut microbiome in PD was identified: altered abundances of three microbial clusters were found, one of which was composed of opportunistic pathogens. Using two large datasets, we show that the overabundance of opportunistic pathogens in PD gut is influenced by the host genotype at the alpha-synuclein locus, and that the variants responsible modulate alpha-synuclein expression. This is the first demonstration of interaction between genetic factors in the human genome and the dysbiosis of gut microbiome in PD.

Genetic studies of the protein kinase AKT1 in Parkinson's disease

2011 ◽  
Vol 501 (1) ◽  
pp. 41-44 ◽  
Author(s):  
Caroline Ran ◽  
Marie Westerlund ◽  
Anna Anvret ◽  
Thomas Willows ◽  
Olof Sydow ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protein Kinase ◽  
Genetic Studies

Deciphering variability in the role of interleukin-1β in Parkinson’s disease

2016 ◽  
Vol 27 (6) ◽  
pp. 635-650 ◽  
Author(s):  
Amene Saghazadeh ◽  
Carina C. Ferrari ◽  
Nima Rezaei
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Disorder ◽  
Mitogen Activated Protein Kinase ◽  
Interleukin 1Β ◽  
Heme Oxygenase 1 ◽  
Genetic Studies ◽  
Mitogen Activated Protein ◽  
Light Chain Enhancer

AbstractAlthough the role of inflammation in neurodegeneration has been well acknowledged, less is known on the issue of each cytokine in specific neurodegenerative diseases. In this review, we will present evidence elucidating that interleukin-1β (IL-1β) has a multi-faceted character in pathogenesis of Parkinson’s disease, which is a progressive neurodegenerative disorder. Increased levels of IL-1β were found in PD patients. Besides, PD symptoms were observed in IL-1β wild-type, but not deficient, animals. These lines of evidence suggest that IL-1β may contribute to the initiation or progression of PD. On the other hand, some studies reported decreased levels of IL-1β in PD patients. Also, genetic studies provided evidence suggesting that IL-1β may protect individuals against PD. Presumably, the broad range of IL-1β role is due to its interaction with both upstream and downstream mediators. Differences in IL-1β levels could be because of glia population (i.e. microglia and astrocytes), mitogen-activated protein kinase and nuclear factor κ light-chain-enhancer of activated B cells signaling pathways, and several mediators (including cyclooxygenase, neurotrophic factors, reactive oxygen species, caspases, heme oxygenase-1, and matrix metalloproteinases). Although far from practice at this point, unraveling theoretical therapeutic targets based on the up-down IL-1β neuroweb could facilitate the development of strategies that are likely to be used for pharmaceutical designs of anti-neurodegenerative drugs of the future.

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