Abstract
Background: Parkinson’s disease (PD) is currently the second most common neurodegenerative disorder, burdening about 10 million elderly individuals worldwide. The multifactorial nature of PD poses a difficult obstacle for understanding the mechanisms involved in its onset and progression. Currently, diagnosis depends on the appearance of clinical signs, some of which are shared among various neurologic disorders, hindering early diagnosis. There are no effective tools to prevent PD onset, detect the disease in early stages or accurately report the risk of disease progression. Hence, there is an increasing demand for biomarkers that may identify disease onset and progression, as treatment-based medicine may not be the best approach for PD. Over the last few decades, the search for molecular markers to predict susceptibility, aid in accurate diagnosis and evaluate the progress of PD have intensified, but strategies aimed to improve individualized patient care have not yet been established. Conclusions: Genomic variation, regulation by epigenomic mechanisms, as well as the influence of the host gut microbiome seem to have a crucial role in the onset and progress of PD, thus are considered potential biomarkers. As such, the human nuclear and mitochondrial genome, epigenome, and the host gut microbiome might be the key elements to the rise of personalized medicine for PD patients.
Highlights
As life expectancy rises as a result of technological advances, humanity faces an increased burden of aging diseases, such as cancer, diabetes, cardiovascular and neurodegenerative disorders
As mitochondrial dysfunctions are believed to play key roles in Parkinson’s disease (PD) progression, the discovery of mitochondrial Piwi-interacting RNAs (piRNAs) in cancer cells [171,172,173] derived from genes involved in the oxidative phosphorylation chain, indicate a more complex regulatory network involving mitochondrial DNA, and is one more reason we should consider investigating the functional roles of piRNAs in healthy central nervous system (CNS) and in disease onset
A review by Cai and Jeong (2020) [240] highlighted that defects in mitophagy have been widely associated with PD and that increased rates of mitochondrial DNA (mtDNA) deletions have been observed in PD patients, which could be related to dysfunctions in this process of mitochondrial quality control
Summary
As life expectancy rises as a result of technological advances, humanity faces an increased burden of aging diseases, such as cancer, diabetes, cardiovascular and neurodegenerative disorders. Most PD patients are diagnosed in late stages, both because of the lack of tools for the evaluation of disease progress risk and the difficulty in differentiating PD from other neurological disorders, since many symptoms of PD overlap with clinical manifestations of other diseases, such as Essential Tremor, Multiple Sclerosis, and Alzheimer’s Disease [12]. The lack of molecular markers to predict susceptibility, accurate diagnosis, and evaluate the progress of PD continues to hinder the establishment of precision medicine strategies. It is essential that we consider the findings of multi-omics approaches, which reveal molecular aspects of PD from multiple perspectives and may lead to the establishment of genetic and epigenetic and other circulating markers, which are less invasive, to be used for accurate diagnosis and clinical management of the disease. We discuss findings concerning the identification and validation of potential genetic, epigenetic and microbial biomarkers to enlighten the state-of-the-art in PD molecular biomarker research
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