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The neuropathology of p. IT mutation was showed to be pure nigral degeneration at the beginning. However, recent report has identified one patient with LBD and one patient with glial cytoplasmic inclusions GCIs whcich highlights the pleomorphic pathology in LRRK2 parkinsonism [ 29 ]. It is perplexing that how one identical mutation in the same kindred can generate different pathologies. For the reason of this occurrence, there are several hypotheses, which are not mutually exclusive. Moreover, the relative balance between an LRRK2 gain of function via kinase dysregulation and aggregation of proteins and loss of function via ERK pathway inactivation or downregulation of protein transcription determines different pathologies.

Clinical features of LRRK2-associated parkinsonism Clinical features resemble those of late-onset sporadic PD, bradykinesia, rigidity, tremor, and good L-dopa response which have been confirmed by clinical and positron emission tomography PET studies. However, female patients carrying the p. Although earlier studies considered tremor as the predominant feature of LRRK2 carriers, in a recent study, tremor was observed less in patients with LRRK2 p. GS than in idiopathic PD [ 30 ]. Analyzing the results of the LRRK2 p. GS exhibited typical levodopa-responsive parkinsonism, with asymmetric onset of symptoms and variable combination of bradykinesia, rigidity and rest tremor [ 31 ].

Moreover, postural tremor was a prominent and early feature. Postural instability and dystonia including unilateral foot dystonia as a presenting symptom were rare, and cognitive abnormalities and autonomic dysfunction were absent.

GS and parkin exon 5 duplication: Consequently, this variability of onset ages could not be explained by genotypes of the APOE gene [ 10 ]. In addition, the phenotype of LRRK2 p. GS mutation paiswn the Argentinean cohort was indistinguishable from patients with idiopathic PD [ 32 ]. Moreover, multiple system atrophy MSA is characterized clinically by parkinsonism, however, p. In addition to the common p. GS carriers, the present study highlights that the distribution in age at onset and clinical features in LRRK2 p. GS parkinsonism, indicating that the effect of mutations in different domains of the LRRK2 protein lead to similar phenotypes [ 34 ].

LRRK2 p.

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RG transgenic mice show decreased locomotors activity which is considered datting hallmark of motor symptoms of PD in human patients. They also display gastrointestinal dysfunction at an early stage but do not have abnormalities in fine behaviors, olfaction, pain sensitivity, mood disorders and learning and memory compared to the controls [ 35 ]. As to patients carrying the p. YC mutation, mainly from a British kindred, showed initially symptoms of asymmetrical rest tremor, and then bradykinesia, rigidity, and postural instability with good reactivity to levodopa treatment [ 36 ].

Unilateral leg tremors at onset and foot dystonia are prominent features in p. YC patients.

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