Leucine-rich repeat kinase-2 (LRRK2) R1441G knockin mice are prone to rotenone-induced mitochondrial dysfunction and dopaminergic cell death

Abstract

Background: Huntington's disease is very rare in Asian country compared with European and American country. This discrepancy is reported by different frequency of haplotypes. Objective: To clarify the prevalence of Huntington's disease in Japan, and to investigate their medical condition. Material and methods: We collected patients' data from Japan Intractable Disease Information Center and department of the specific disease control, Japanese Ministry of Health, Labor and Welfare. Then, we analyzed these data with statistical methods.

LRRK2-G2019S Synergizes with Ageing and Low-Grade Inflammation to Promote Gut and Peripheral Immune Cell Activation that Precede Nigrostriatal Degeneration

“…[18][19][20][21][109][110][111] Overexpression (OE) of pathogenic LRRK2 mutants, such as G2019S, R1441C, or R1441G, induces PD-like phenotypes, including age-dependent DA neuronal loss, disruption of dopamine homeostasis, L-DOPA responsive locomotor defects, and pathological accumulations of tau and α-syn. 15,[112][113][114][115][116][117] While OE models enable the investigation of PD neurodegenerative features, they are limited by potential overexpressionrelated artifacts. Previous studies have also examined the combined effect of ageing, environmental toxicity, and LRRK2related genetic vulnerability.…”

LRRK2-G2019S Synergizes With Ageing and Low-Grade Inflammation to Promote Gut and Peripheral Immune Cell Activation That Precede Nigrostriatal Degeneration

“…[18][19][20][21][110][111][112] Overexpression (OE) of pathogenic LRRK2 mutants, such as G2019S, R1441C, or R1441G, induces PD-like phenotypes, including age-dependent DA neuronal loss, disruption of dopamine homeostasis, L-DOPA responsive locomotor defects, and pathological accumulations of tau and α-syn. 15,[113][114][115][116][117][118] While OE models enable the investigation of PD neurodegenerative features, they are limited by potential overexpression-related artifacts. Previous studies have also examined the combined effect of ageing, environmental toxicity, and LRRK2-related genetic vulnerability.…”