LRRK2 and parkin immunoreactivity in multiple system atrophy inclusions View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2008-10-21

AUTHORS

Yue Huang, Yun Ju Christine Song, Karen Murphy, Janice L. Holton, Tammaryn Lashley, Tamas Revesz, Wei-Ping Gai, Glenda Margaret Halliday

ABSTRACT

Certain genetic defects in LRRK2 and parkin are pathogenic for Parkinson’s disease (PD) and both proteins deposit in the characteristic Lewy bodies. LRRK2 is thought to be involved in the early initiation of Lewy bodies. The involvement of LRRK2 and parkin in the similar cellular deposition of fibrillar α-synuclein in glial cytoplasmic inclusions (GCI) in multiple system atrophy (MSA) has not yet been assessed. To determine whether LRRK2 and parkin may be similarly associated with the abnormal deposition of α-synuclein in MSA GCI, paraffin-embedded sections from the basal ganglia of 12 patients with MSA, 4 with PD and 4 controls were immunostained for LRRK2, parkin, α-synuclein and oligodendroglial proteins using triple labelling procedures. The severity of neuronal loss was graded and the proportion of abnormally enlarged oligodendroglia containing different combinations of proteins assessed in 80–100 cells per case. Parkin immunoreactivity was observed in only a small proportion of GCI. In contrast, LRRK2 was found in most of the enlarged oligodendroglia in MSA and colocalised with the majority of α-synuclein-immunopositive GCI. Degrading myelin sheaths containing LRRK2-immunoreactivity were also observed, showing an association with one of the earliest oligodendroglial abnormalities observed in MSA. The proportion of LRRK2-immunopositive GCI was negatively associated with an increase in neuronal loss and α-synuclein-immunopositive dystrophic axons. Our results indicate that an increase in LRRK2 expression occurs early in association with myelin degradation and GCI formation, and that a reduction in LRRK2 expression in oligodendroglia is associated with increased neuronal loss in MSA. More... »

PAGES

639

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00401-008-0446-3

DOI

http://dx.doi.org/10.1007/s00401-008-0446-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1024715594

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18936941


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37 schema:description Certain genetic defects in LRRK2 and parkin are pathogenic for Parkinson’s disease (PD) and both proteins deposit in the characteristic Lewy bodies. LRRK2 is thought to be involved in the early initiation of Lewy bodies. The involvement of LRRK2 and parkin in the similar cellular deposition of fibrillar α-synuclein in glial cytoplasmic inclusions (GCI) in multiple system atrophy (MSA) has not yet been assessed. To determine whether LRRK2 and parkin may be similarly associated with the abnormal deposition of α-synuclein in MSA GCI, paraffin-embedded sections from the basal ganglia of 12 patients with MSA, 4 with PD and 4 controls were immunostained for LRRK2, parkin, α-synuclein and oligodendroglial proteins using triple labelling procedures. The severity of neuronal loss was graded and the proportion of abnormally enlarged oligodendroglia containing different combinations of proteins assessed in 80–100 cells per case. Parkin immunoreactivity was observed in only a small proportion of GCI. In contrast, LRRK2 was found in most of the enlarged oligodendroglia in MSA and colocalised with the majority of α-synuclein-immunopositive GCI. Degrading myelin sheaths containing LRRK2-immunoreactivity were also observed, showing an association with one of the earliest oligodendroglial abnormalities observed in MSA. The proportion of LRRK2-immunopositive GCI was negatively associated with an increase in neuronal loss and α-synuclein-immunopositive dystrophic axons. Our results indicate that an increase in LRRK2 expression occurs early in association with myelin degradation and GCI formation, and that a reduction in LRRK2 expression in oligodendroglia is associated with increased neuronal loss in MSA.
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45 LRRK2
46 LRRK2 expression
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48 LRRK2-immunoreactivity
49 Lewy bodies
50 MSA GCI
51 Parkin
52 Parkinson's disease
53 abnormal deposition
54 abnormalities
55 association
56 atrophy
57 atrophy inclusions
58 axons
59 basal ganglia
60 body
61 cases
62 cells
63 cellular deposition
64 certain genetic defects
65 characteristic Lewy bodies
66 combination
67 contrast
68 control
69 cytoplasmic inclusions
70 defects
71 degradation
72 deposition
73 different combinations
74 disease
75 dystrophic axons
76 earliest oligodendroglial abnormalities
77 early initiation
78 expression
79 formation
80 ganglia
81 genetic defects
82 glial cytoplasmic inclusions
83 immunoreactivity
84 inclusion
85 increase
86 initiation
87 involvement
88 involvement of LRRK2
89 labeling procedure
90 loss
91 majority
92 multiple system atrophy
93 multiple system atrophy inclusions
94 myelin degradation
95 myelin sheath
96 neuronal loss
97 oligodendroglia
98 oligodendroglial abnormalities
99 oligodendroglial protein
100 paraffin
101 parkin immunoreactivity
102 patients
103 procedure
104 proportion
105 protein
106 reduction
107 results
108 sections
109 severity
110 sheath
111 similar cellular deposition
112 small proportion
113 synuclein
114 synuclein-immunopositive GCI
115 synuclein-immunopositive dystrophic axons
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