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The expression of DJ-1 (PARK7) in normal human CNS and idiopathic Parkinson's disease.
TLDR
It is concluded that DJ-1 is not an essential component of LBs and Lewy neurites, is expressed mainly by astrocytes in human brain tissue and is sensitive to oxidative stress conditions, consistent with the hypothesis that neuronal-glial interactions are important in the pathophysiology of Parkinson's disease.
Contractile proteins in pericytes at the blood-brain and blood-retinal barriers
TLDR
Support is added for a contractile role in pericytes of the CNS microvasculature, similar to that of vascular smooth muscle cells, in the regulation of capillary blood flow.
Pathological inclusion bodies in tauopathies contain distinct complements of tau with three or four microtubule‐binding repeat domains as demonstrated by new specific monoclonal antibodies
TLDR
Two monoclonal antibodies, RD3 and RD4, are developed that effectively distinguish these closely related tau isoforms that are useful tools for analysing t Tau isoform expression and distribution as well as pathological changes in the human brain.
α-Synuclein fate is determined by USP9X-regulated monoubiquitination
TLDR
The data indicate that monoubiquitination is a key determinant of α-synuclein fate, and lower levels of cytosolic USP9X and deubiquitinase activity in α- synucleinopathies may contribute to the accumulation and aggregation of monoubiqueitinated α- Synuclein in Lewy bodies.
A comparative clinical, pathological, biochemical and genetic study of fused in sarcoma proteinopathies.
TLDR
There is considerable overlap and also significant differences in fused in sarcoma-positive pathology between the two subgroups, suggesting they may represent a spectrum of the same disease.
Globular glial tauopathies (GGT) presenting with motor neuron disease or frontotemporal dementia: an emerging group of 4-repeat tauopathies
TLDR
The term globular glial tauopathy is proposed as an encompassing term to classify this emerging class of 4R t Tauopathy, which has overlapping pathological features with progressive supranuclear palsy but present with clinical features of motor neuron disease and/or frontotemporal dementia.
Parkinson's disease-linked mutations in VPS35 induce dopaminergic neurodegeneration
TLDR
It is established that dominant V PS35 mutations lead to neurodegeneration in PD consistent with a gain-of-function mechanism, and support a key role for VPS35 in the development of PD.
SUMOylation and ubiquitination reciprocally regulate α-synuclein degradation and pathological aggregation
TLDR
A marked increase in PIAS2 expression along with SUMOylated α-synuclein in PD brains is detected, providing a causal mechanism underlying the up-regulation of α- SynucleinsumOylation in the disease.
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