A common leucine-rich repeat kinase 2 gene mutation in familial and sporadic Parkinson's disease in Russia.

doi:10.1111/j.1468-1331.2007.01685.x

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Back to search

Article

A common leucine-rich repeat kinase 2 gene mutation in familial and sporadic Parkinson's disease in Russia.

European journal of neurology - 1 Apr 2007

Illarioshkin S N, Shadrina M I, Slominsky P A, Bespalova E V, Zagorovskaya T B, Bagyeva G Kh, Markova E D, Limborska S A, Ivanova-Smolenskaya I A

Abstract excerpt

A PARK8 form of Parkinson's disease (PD) is caused by a novel gene, leucine-rich repeat kinase 2 (LRRK2), and a single mutation G2019S was found in a proportion of LRRK2-associated cases of diverse ethnic origins. We performed the LRRK2 G2019S mutation analysis in 304 Russian patients with PD, in...

Topics

Adult
Age of Onset
Aged
DNA Mutational Analysis
Female
Founder Effect
Gene Frequency
Genetic Predisposition to Disease
Genotype
Heterozygote
Humans
Leucine-Rich Repeat Serine-Threonine Protein Kinase-2

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Male

Middle Aged

Mutation

Parkinson Disease

Protein Serine-Threonine Kinases

Reverse Transcriptase Polymerase Chain Reaction

Source

Open in PubMed

Identifiers

PMID: 17388990
DOI: 10.1111/j.1468-1331.2007.01685.x

Genes

APOE

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026. Prepared record publication-17388990-2026-08-30.1. Manifest publication-graph-cohort-2026-08-30.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 30 Aug 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

discussions

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A common leucine-rich repeat kinase 2 gene mutation in familial and sporadic Parkinson's disease in Russia.PMID 17388990Read ↗

G2019S LRRK2 mutation in familial and sporadic Parkinson's disease in Russia.Semantic proximity Read ↗

[A PARK8 form of Parkinson's disease: a mutational analysis of the LRRK2 gene in Russian population].Semantic proximity Read ↗

Screening for LRRK2 mutations in patients with Parkinson's disease in Russia: identification of a novel LRRK2 variant.Semantic proximity Read ↗

Identification of a novel LRRK2 mutation linked to autosomal dominant parkinsonism: evidence of a common founder across European populations.Semantic proximity Read ↗

LRRK2 in Parkinson's disease: genetic and clinical studies from patients.Semantic proximity Read ↗

A study of LRRK2 mutations and Parkinson's disease in Brazil.Semantic proximity Read ↗

High prevalence of LRRK2 mutations in familial and sporadic Parkinson's disease in Portugal.Semantic proximity Read ↗

Leucine-Rich Repeat Kinase (LRRK2) Genetics and Parkinson's Disease.Semantic proximity Read ↗

The G6055A (G2019S) mutation in LRRK2 is frequent in both early and late onset Parkinson's disease and originates from a common ancestor.Semantic proximity Read ↗

LRRK2 low-penetrance mutations (Gly2019Ser) and risk alleles (Gly2385Arg)-linking familial and sporadic Parkinson's disease.Semantic proximity Read ↗

Mutation analysis of Parkinson's disease genes in a Russian data set.Semantic proximity Read ↗

G2019S mutation of the leucine-rich repeat kinase 2 gene in a cohort of Egyptian patients with Parkinson's disease.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.