scholarly journals Leucine-Rich Repeat Kinase 2-Linked Parkinson’s Disease: Clinical and Molecular Findings

2010 ◽  
Vol 3 (2) ◽  
pp. 25-31 ◽  
Author(s):  
Udhaya Kumari ◽  
Eng-King Tan
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Leucine Rich Repeat

scholarly journals Effect of a Leucine-rich Repeat Kinase 2 Variant on Motor and Non-motor Symptoms in Chinese Parkinson’s Disease Patients

2016 ◽  
Vol 7 (3) ◽  
pp. 230 ◽  
Author(s):  
Qian Sun ◽  
Tian Wang ◽  
Tian-Fang Jiang ◽  
Pei Huang ◽  
Dun-Hui Li ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Motor Symptoms ◽  
Leucine Rich Repeat ◽  
Non Motor Symptoms

scholarly journals Leucine-Rich Repeat Kinase 2 in Parkinson’s Disease: Updated from Pathogenesis to Potential Therapeutic Target

2018 ◽  
Vol 79 (5-6) ◽  
pp. 256-265 ◽  
Author(s):  
Jinhua Chen ◽  
Ying Chen ◽  
Jiali Pu
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Significant Role ◽  
Dopaminergic Neurons ◽  
Recent Progress ◽  
Therapeutic Agents ◽  
Leucine Rich Repeat ◽  
Potential Therapeutic Target ◽  
Genetic And Environmental Factors

Background: Parkinson’s disease (PD) is characterized by the selective loss of dopaminergic neurons in the midbrain. The pathogenesis of PD is not fully understood but is likely caused by a combination of genetic and environmental factors. Several genes are associated with the onset and progression of familial PD. There is increasing evidence that leucine-rich repeat kinase 2 (LRRK2) plays a significant role in PD pathophysiology. Summary: Many studies have been conducted to elucidate the functions of LRRK2 and identify effective LRRK2 inhibitors for PD treatment. In this review, we discuss the role of LRRK2 in PD and recent progress in the use of LRRK2 inhibitors as therapeutic agents. Key Messages: LRRK2 plays a significant role in the pathophysiology of PD, and pharmacological inhibition of LRRK2 has become one of the most promising potential therapies for PD. Further research is warranted to determine the functions of LRRK2 and expand the applications of LRRK2 inhibitors in PD treatment.

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.

scholarly journals The Parkinson’s disease-linked Leucine-rich repeat kinase 2 (LRRK2) is required for insulin-stimulated translocation of GLUT4

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Natalja Funk ◽  
Marita Munz ◽  
Thomas Ott ◽  
Kathrin Brockmann ◽  
Andrea Wenninger-Weinzierl ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Leucine Rich Repeat

Neuronal microtubules and proteins linked to Parkinson’s disease: a relevant interaction?

2019 ◽  
Vol 400 (9) ◽  
pp. 1099-1112 ◽  
Author(s):  
Alessandra M. Calogero ◽  
Samanta Mazzetti ◽  
Gianni Pezzoli ◽  
Graziella Cappelletti
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Intracellular Trafficking ◽  
Gene Mutations ◽  
Neuronal Loss ◽  
Leucine Rich Repeat ◽  
Microtubule Cytoskeleton ◽  
Pathological Conditions ◽  
Toxin Exposure ◽  
Relevant Interaction

AbstractNeuronal microtubules are key determinants of cell morphology, differentiation, migration and polarity, and contribute to intracellular trafficking along axons and dendrites. Microtubules are strictly regulated and alterations in their dynamics can lead to catastrophic effects in the neuron. Indeed, the importance of the microtubule cytoskeleton in many human diseases is emerging. Remarkably, a growing body of evidence indicates that microtubule defects could be linked to Parkinson’s disease pathogenesis. Only a few of the causes of the progressive neuronal loss underlying this disorder have been identified. They include gene mutations and toxin exposure, but the trigger leading to neurodegeneration is still unknown. In this scenario, the evidence showing that mutated proteins in Parkinson’s disease are involved in the regulation of the microtubule cytoskeleton is intriguing. Here, we focus on α-Synuclein, Parkin and Leucine-rich repeat kinase 2 (LRRK2), the three main proteins linked to the familial forms of the disease. The aim is to dissect their interaction with tubulin and microtubules in both physiological and pathological conditions, in which these proteins are overexpressed, mutated or absent. We highlight the relevance of such an interaction and suggest that these proteins could trigger neurodegeneration via defective regulation of the microtubule cytoskeleton.

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