Altered Gut Microbiome in Parkinson’s Disease and the Influence
of Lipopolysaccharide in a Human α-Synuclein Over-Expressing Mouse Model
Highlights
The interaction
between the gut microbiota and alpha-synuclein (αSyn) aggregation in
Parkinson’s disease (PD) is receiving increasing attention. The objective of
this study was to investigate gut microbiota, and effects of an inflammatory
lipopolysaccharide (LPS) trigger in a human αSyn over-expressing mouse model of
PD (Thy1-αSyn).
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Proteomic studies associated with Parkinson’s disease
Highlights
The number of
publications relating to the proteomics of PD is vast. Therefore, there is a
need to evaluate the current proteomics literature and establish the connections
between the past and the present to foresee the future.
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Role of the ubiquitin proteasome system in Parkinson's disease
Highlights
Recently, several
lines of evidence have implicated an intimate link between aberrations in the
ubiquitin proteasome system (UPS) and PD pathogenesis. Derangements of the UPS,
which normally functions as a type of protein degradation machinery, lead to
alterations in protein homeostasis that could conceivably promote the toxic accumulation of proteins detrimental to neuronal survival.
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The roles of non-coding RNAs in Parkinson’s disease
Highlights
Up until now, many de
novo investigations have been conducted to disclose the mechanisms underlying
in PD. Among them, impacts of non-coding RNAs (ncRNAs) on the pathogenesis
and/or progression of PD need to be highlighted. microRNAs (miRNAs) and long
ncRNAs (lncRNAs) are more noteworthy in this context.
Defective mitochondrial DNA homeostasis in the substantia nigra
in Parkinson disease
Highlights
Here, we study the
complete spectrum of mtDNA changes, including deletions, copy-number variation
and point mutations, in single neurons from the dopaminergic
substantia nigra
and other brain areas of individuals with Parkinson disease and neurologically
healthy controls.
The interplay of aging, genetics and environmental factors in
the pathogenesis of
Parkinson’s disease
Parkinson’s disease
(PD) is characterized by dopaminergic neuronal loss in the substantia nigra
pars compacta and intracellular inclusions called Lewy bodies (LB). During the
course of disease, misfolded α-synuclein, the major constituent of LB, spreads to
different regions of the brain in a prion-like fashion, giving rise to
successive non-motor and motor symptoms. Etiology is likely multifactorial, and
involves interplay among aging, genetic susceptibility and environmental
factors.
Genetic risk factors in
Parkinson’s disease
Over the last two
decades, we have witnessed a revolution in the field of Parkinson’s disease
(PD) genetics. Great advances have been made in identifying many loci that
confer a risk for PD, which has subsequently led to an improved understanding
of the molecular pathways involved in disease pathogenesis. Despite this
success, it is predicted that only a relatively small proportion of the
phenotypic variability has been explained by genetics.
Epigenetic Study in Parkinson’s Disease: A Pilot Analysis of DNA
Methylation in Candidate Genes in Brain
Efforts have been
made to understand the pathophysiology of Parkinson’s disease (PD). A
significant number of studies have focused on genetics, despite the fact that
the described pathogenic mutations have been observed only in around 10% of
patients; this observation supports the fact that PD is a multifactorial
disorder.
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Epigenetic Biomarkers for
Parkinson’s Disease: From
Diagnostics to Therapeutics
Parkinson’s disease
(PD) is a prevalent neurodegenerative illness that is often diagnosed after
significant pathology and neuronal cell loss has occurred. Biomarkers of PD are
greatly needed for early diagnosis, as well as for the prediction of disease
progression and treatment outcome. In this regard, the epigenome, which is
partially dynamic, holds
considerable promise for the development of molecular
biomarkers for PD.
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