Article
Neurodegenerative phenotypes in an A53T α-synuclein transgenic mouse model are independent of LRRK2.
Human molecular genetics - 1 Jun 2012
Daher João Paulo L, Pletnikova Olga, Biskup Saskia, Musso Alessandra, Gellhaar Sandra, Galter Dagmar, Troncoso Juan C, Lee Michael K, Dawson Ted M, Dawson Valina L, Moore Darren J
Abstract excerpt
Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD. LRRK2 mutations cause late-onset familial PD with a clinical, neurochemical and, for the most...
Topics
- Animals
- Brain
- Disease Models, Animal
- Humans
- Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
- Lewy Bodies
- Mice
- Mice, Knockout
- Mice, Transgenic
- Neurodegenerative Diseases