ReviewExperimental neurobiology2013
LRRK2 as a Potential Genetic Modifier of Synucleinopathies: Interlacing the Two Major Genetic Factors of Parkinson's Disease.
Review in Experimental neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Longitudinal decline in striatal DAT binding in LRRK2 Parkinson's disease: connections with CSF α-synuclein seeding activity.Journal of neurology · 2025Article
- Expanding our understanding of synucleinopathies: proteinopathy, proteinopenia, and lipidopathy.The FEBS journal · 2025Review
- A genome-wide association study identifies a novel East Asian-specific locus for dementia with Lewy bodies in Japanese subjects.Molecular medicine (Cambridge, Mass.) · 2025Article
- Prion-Like Mechanisms in Parkinson's Disease.Frontiers in neuroscience · 2019Review
- LRRK2 G2019S Mutation Inhibits Degradation of α-Synuclein in an In Vitro Model of Parkinson's Disease.Current medical science · 2018Article
- A clinicopathological approach to the diagnosis of dementia.Nature reviews. Neurology · 2017Review
- LRRK2 inhibitors and their potential in the treatment of Parkinson's disease: current perspectives.Clinical pharmacology : advances and applications · 2016Review
- Lewy body dementias.Lancet (London, England) · 2015Review
- ATP13A2/PARK9 Deficiency Neither Cause Lysosomal Impairment Nor Alter α-Synuclein Metabolism in SH-SY5Y Cells.Experimental neurobiology · 2014Article
- Membrane recruitment of endogenous LRRK2 precedes its potent regulation of autophagy.Human molecular genetics · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) and related Lewy body diseases are characterized by deposition of α-synuclein aggregates in both the central nervous system and peripheral nervous system. Synucleinopathy lesions spread to larger brain areas as the disease progresses, and prion-like cell-to-cell transmission of aggregated α-synuclein is thought to be the underlying mechanism for this pathological spreading. LRRK2 is another protein linked to the pathogenesis of PD, and its presence in Lewy bodies has attracted much attention as to whether LRRK2 and α-synuclein interplay during the pathogenesis of PD. However, the relationship between these two crucial proteins still remains unclear. In this review article, we will discuss the current state of knowledge in terms of how these proteins cause the disease and provide the hypothetical mechanisms by which LRRK2 might modify the generation and progression of synucleinopathy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.