TAILIEUCHUNG - Báo cáo khoa học: Emerging pathways in genetic Parkinson’s disease: tangles, Lewy bodies and LRRK2

The last decade has seen clear links emerge between the genetic determi-nants and neuropathological hallmarks of parkinsonism and dementia, notably with the discovery of mutations ina-synuclein and tau. Following the description of mutations in LRRK2 linked to Parkinson’s disease, char-acterized by variable pathology including eithera-synuclein or tau deposi-tion, it has been suggested that LRRK2 functions as an upstream regulator of Parkinson’s disease pathogenesis. | MINIREVIEW Emerging pathways in genetic Parkinson s disease tangles Lewy bodies and LRRK2 Michael J. Devine1 and Patrick A. Lewis2 1 Department of ClinicalNeuroscience Imperial college London UK 2 Department of Molecular Neuroscience Institute of Neurology University College London UK Keywords a-synuclein Lewy bodies LRRK2 MAPT neurofibrillary tangles paired helical filament Parkinson s disease ROCO protein SNCA tau Correspondence P. A. Lewis Department of Molecular Neuroscience Institute of Neurology University College London Queen Square London WC1N 3bG UK Fax 44 0207 833 1016 Tel 44 0207 829 8722 Received 7 July 2008 revised 2 September 2008 accepted 24 September 2008 doi The last decade has seen clear links emerge between the genetic determinants and neuropathological hallmarks of parkinsonism and dementia notably with the discovery of mutations in a-synuclein and tau. Following the description of mutations in LRRK2 linked to Parkinson s disease characterized by variable pathology including either a-synuclein or tau deposition it has been suggested that LRRK2 functions as an upstream regulator of Parkinson s disease pathogenesis. This minireview explores this model in the context of our current understanding of the biochemistry of LRRK2 a-synuclein and tau. Introduction Parkinson s disease PD is characterized by tremor rigidity and difficulty initiating movement 1 . It is the most common neurodegenerative movement disorder estimated to affect 100-180 per 100 000 with prevalence rising with age. The economic burden in the UK alone is 6 billion per annum 2 . The pathological hallmark of PD is depigmentation of the substantia nigra pars compacta SNpc representing loss of dopaminergic neurons. Abnormal fibrillar cytoplasmic inclusions Lewy bodies LBs are seen in surviving nigrostriatal neurons at autopsy and these have to be present for a diagnosis of PD to be made 3 . Although the clinical and .

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