Abstract
When James Parkinson described the classical symptoms of the disease he could hardly foresee the evolution of our understanding over the next two hundred years. Nowadays, Parkinson’s disease is considered a complex multifactorial disease in which genetic factors, either causative or susceptibility variants, unknown environmental cues, and the potential interaction of both could ultimately trigger the pathology. Noteworthy advances have been made in different fields from the clinical phenotype to the decoding of some potential neuropathological features, among which are the fields of genetics, drug discovery or biomaterials for drug delivery, which, though recent in origin, have evolved swiftly to become the basis of research into the disease today. In this review, we highlight some of the key advances in the field over the past two centuries and discuss the current challenges focusing on exciting new research developments likely to come in the next few years. Also, the importance of pre-motor symptoms and early diagnosis in the search for more effective therapeutic options is discussed.
Highlights
Reviewed by: Yoland Smith, Emory University, United States Marco Aurelio M
The nanoformulation was able to attenuate MPTP-induced lipid peroxidation and prevent striatal tyrosine hydroxylase (TH) protein decrease in parkinsonian mice. These findings suggest that resveratrol-loaded NPs are a promising nanomedical tool for Parkinson’s Disease (PD)
Population aging in developed countries will increase the burden of neurodegenerative diseases
Summary
The etiology of PD remains largely unknown. The majority of patients are classified as idiopathic PD cases, i.e., arising ‘spontaneously’ or from an unknown cause. Pathogenic mutations in the genes ATPase 13A2 (ATP13A2) (Bras et al, 2012), phospholipase A2 (PLA2G6) (Gregory et al, 2008) F-Box protein 7 (FBXO7) (Shojaee et al, 2008), DNA J Heat Shock Protein Family (Hsp40) Member C6 (DNAJC6) (Edvardson et al, 2012) and Vacuolar Protein Sorting 13 Homolog C (VPS13C) (Lesage et al, 2016) are linked to autosomal recessive, early-onset atypical parkinsonism that often comprises additional clinical features such as pyramidal degeneration, ataxia or dementia, with or without LBs. Overall, the relative contribution of pathogenic mendelian genes to overall PD is limited, genetic research in PD has been instrumental since it has uniquely permitted the identification of disease molecular alterations, pathophysiological pathways, and candidate therapeutic targets, most of which are believed to be largely common to sPD. GBA-mutation carriers show a more severe parkinsonism than idiopathic patients, earlier ageat-onset and more frequently dementia (Thaler et al, 2017)
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