Correction to: Concordance analysis of microarray studies identifies representative gene expression changes in Parkinson’s disease: a comparison of 33 human and animal studies

Since the first description of Parkinson's disease (PD) nearly two centuries ago, a number of studies have revealed the clinical symptoms, pathology, and therapeutic approaches to overcome this intractable neurodegenerative disease. 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) are neurotoxins which produce Parkinsonian pathology. From the animal studies using these neurotoxins, it has become well established that oxidative stress is a primary cause of, and essential for, cellular apoptosis in dopaminergic neurons. Here, we describe the mechanism whereby oxidative stress evokes irreversible cell death, and propose a novel therapeutic strategy for PD using molecular hydrogen. Hydrogen has an ability to reduce oxidative damage and ameliorate the loss of nigrostriatal dopaminergic neuronal pathway in two experimental animal models. Thus, it is strongly suggested that hydrogen might provide a great advantage to prevent or minimize the onset and progression of PD.

Download Full-text

The Effect of Dopamine on Gene Expression of Alpha-synuclein and Transcription Factors GATA-1, GATA-2, and ZSCAN21 in Parkinson’s Disease

Cell and Tissue Biology ◽

10.1134/s1990519x18050024 ◽

2018 ◽

Vol 12 (5) ◽

pp. 410-418

Author(s):

A. K. Emelyanov ◽

A. O. Lavrinova ◽

E. M. Litusova ◽

N. A. Knyazev ◽

D. G. Kulabukhova ◽

...

Keyword(s):

Gene Expression ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Transcription Factors ◽

Alpha Synuclein

Download Full-text

Gene expression of the nicotinic acetylcholine receptor α4 subunit in the frontal cortex in Parkinson's disease patients

Neuroscience Letters ◽

10.1016/0304-3940(95)11367-6 ◽

1995 ◽

Vol 187 (3) ◽

pp. 173-176 ◽

Cited By ~ 14

Author(s):

Hannsjörg Schröder ◽

Robert A.I. de Vos ◽

Ernst N.H. Jansen ◽

Christina Birtsch ◽

Andrea Wevers ◽

...

Keyword(s):

Gene Expression ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Frontal Cortex ◽

Acetylcholine Receptor ◽

Nicotinic Acetylcholine Receptor ◽

Nicotinic Acetylcholine

Download Full-text

The universal non-neuronal nature of Parkinson's disease: A theory

10.7287/peerj.preprints.1314v1 ◽

2015 ◽

Author(s):

André Valente ◽

Altynay Adilbayeva ◽

Tursonjan Tokay ◽

Albert Rizvanov

Keyword(s):

Gene Expression ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Mitochondrial Dna ◽

Late Onset ◽

Clinical Signs ◽

Global Gene Expression ◽

Neuron Death ◽

Hematopoietic Stem ◽

Hematopoietic Stem Cell Niche

Various recent developments of relevance to Parkinson's disease (PD) are discussed and integrated into a comprehensive hypothesis on the nature, origin and inter-cellular mode of propagation of late-onset sporadic PD. We propose to define sporadic PD as a characteristic pathological deviation in the global gene expression program of a cell: the PD expression-state, or PD-state for short. Although a universal cell-generic state, the PD-state deviation would be particularly damaging in a neuronal context, ultimately leading to neuron death and the ensuing observed clinical signs. We review why age accumulated damage caused by oxidative stress in mitochondria could be the trigger for a primordial cell to shift to the PD-state. We put forward hematopoietic cells could be the first to acquire the PD-state, at hematopoiesis, from the disruption in reactive oxygen species (ROS) homeostasis that arises with age in the hematopoietic stem-cell niche. We argue why, nonetheless, such a process is unlikely to explain the shift to the PD-state of all the subsequently affected cells in a patient, thus indicating the existence of a distinct mechanism of propagation of the PD-state. We highlight recent findings on the intercellular exchange of mitochondrial DNA and the ability of mitochondrial DNA to modulate the cellular global gene expression state and propose this could form the basis for the intercellular propagation of the PD-state.

Download Full-text

Molecular and functional variation in iPSC-derived sensory neurons

10.1101/095943 ◽

2017 ◽

Cited By ~ 3

Author(s):

Jeremy Schwartzentruber ◽

Stefanie Foskolou ◽

Helena Kilpinen ◽

Julia Rodrigues ◽

Kaur Alasoo ◽

...

Keyword(s):

Gene Expression ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Chromatin Accessibility ◽

Nervous System Development ◽

Sensory Function ◽

Neuronal Cultures ◽

Common Disease ◽

Specific Method ◽

Causal Variants

AbstractInduced pluripotent stem cells (iPSCs), and cells derived from them, have become key tools to model biological processes and disease mechanisms, particularly in cell types such as neurons that are difficult to access from living donors. Here, we present the first map of regulatory variants in an iPSC-derived cell type. To investigate genetic contributions to human sensory function, we performed 123 differentiations of iPSCs from 103 unique donors to a sensory neuronal fate, and measured gene expression, chromatin accessibility, and neuronal excitability. Compared with primary dorsal root ganglion, where sensory nerves collect near the spinal cord, gene expression was more variable across iPSC-derived neuronal cultures, particularly in genes related to differentiation and nervous system development. Single cell RNA-sequencing revealed that although the majority of cells are neuronal and express the expected marker genes, a substantial fraction have a fibroblast-like expression profile. By applying an allele-specific method we identify 3,778 quantitative trait loci influencing gene expression, 6,318 for chromatin accessibility, and 2,097 for RNA splicing at FDR 10%. A number of these overlap with common disease associations, and suggest candidate causal variants and target genes. These include known causal variants at SNCA for Parkinson’s disease and TNFRSF1A for multiple sclerosis, as well as new candidates for migraine, Parkinson’s disease, and schizophrenia.

Download Full-text