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- W2034754214 abstract "Parkinson's disease (PD) is characterised by depigmentation of the substantia nigra, caused by selective and progressive loss of dopaminergic neurons, and the presence of Lewy bodies (a key component of which is α-synuclein) within the surviving neurons of the substantia nigra and other brain regions. LRRK2 mutations are the most common cause of autosomal dominant PD and parkinsonism, and also occur in sporadic forms of the disease. Yet, many cases of what is typically thought of as a “synucleinopathy” have a higher than expected level of tau pathology compared to controls. The converse is true for Alzheimer's disease (AD), where a four fold increase in Lewy bodies has been seen in sporadic cases of AD compared with controls. Additionally Novartis has recently patented LRRK2 polymorphisms as biomarkers for conversion of Mild Cognitive Impairment to AD. This led us to hypothesize that LRRK2 may represent a common link between tauopathies and synucleinopathies. Although direct interaction has not been established between tau and LRRK2, we decided to investigate the possibility of an interaction using transgenic mice with both inducible human P301L tau expressed in the forebrain and either mutant (G2019S) or wild-type human LRRK2. Mice have been analyzed by immunohistochemistry and Western blots for the impact of wild-type or mutant human LRRK2 on abnormal tau neuropathology and biochemical changes. Inducible tau transgenic mice (rTg4510) develop pretangle pathology at 2.5M and mature tangles at 4M and 5.5M of age in the cortex and hippocampus, respectively. We have bred the rTg4510 line with BAC transgenic mice expressing either mutant (G2019S) or wild-type human LRRK2 and have aged them to these same timepoints. Initial analysis of one animal of each genotype at 4M and 5.5M indicates that overexpression of wild-type LRRK2 may delay the progression of tauopathy, resulting in fewer mature tangles and prolonged axonal localization of tau. Initial analysis of wild-type LRRK2 mice on the rTg4510 background suggests that LRRK2 may be protective against tauopathy. Data from larger aged cohorts as well as from the mutant LRRK2 mice on the rTg4510 background will be presented at the conference." @default.
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- W2034754214 date "2008-07-01" @default.
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- W2034754214 title "P1-106: LRRK2 as a common link between tauopathies and synucleinopathies" @default.
- W2034754214 doi "https://doi.org/10.1016/j.jalz.2008.05.693" @default.
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