Cloning of the gene containing mutations that cause PARK8-linked Parkinson's disease.

By C. Paisán-Ruiz, S. Jain, E. Evans, W. Gilks, J. Simon, M. V. D. Brug, A. L. Munain, Silvia Aparicio, N. Khan, Janel O. Johnson and 9 more. Neuron, 2004

2,454 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/5be1cd53d460e14b9c50659413f40fc7b4e2411f

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In Cellular and Molecular Neuroscience

In Neurology

Citations in the corpus

The genetic epidemiology of neurodegenerative disease. (2005, background): “AD APP (15) Aβ precursor protein 21q21 Dominant Altered Aβ production (Aβ42/Aβ40 ratio ↑) and aggregation AD APOE (21, 22) Apolipoprotein E 19q13 Risk factor Unknown (Aβ aggregation? lipid metabolism?) AD PSEN1 (16) Presenilin 1 14q24 Dominant Altered Aβ production (Aβ42/Aβ40 ratio ↑) AD PSEN2 (17, ”
LRRK2 Mutant iPSC-Derived DA Neurons Demonstrate Increased Susceptibility to Oxidative Stress (2011, positive): “Moreover, although transgenic animal and cell models expressing known PD-associated genes have provided important insights into the disease (Betarbet et al., 2002; Heo et al., 2010; Ng et al., 2009; Paisan-Ruiz et al., 2004; Schüle et al., 2009), it has been difficult to demonstrate that implicated ”
Epidemiology and etiology of Parkinson’s disease: a review of the evidence (2011, background): “Two research groups independently found mutations in the LRRK2 gene in several families with autosomal dominant PD of different origin [175, 184].”
Neuroinflammation in Parkinson’s disease and its potential as therapeutic target (2015, background): “In the last several years, the common variations in leucine-rich repeat kinase 2 (LRRK2) gene have been identified as risk factors of both familial and sporadic PD [67–70].”