Abstract
Parkinson’s disease (PD) is a progressive neurodegenerative disorder that is characterized by a loss of dopaminergic neurons, leading to bradykinesia, rigidity, tremor at rest, and postural instability, as well as non-motor symptoms such as olfactory impairment, pain, autonomic dysfunction, impaired sleep, fatigue, and behavioral changes. The pathogenesis of PD is believed to involve oxidative stress, disruption to mitochondria, alterations to the protein α-synuclein, and neuroinflammatory processes. There is currently no cure for the disease. Polyphenols are secondary metabolites of plants, which have shown benefit in several experimental models of PD. Intake of polyphenols through diet is also associated with lower PD risk in humans. In this review, we provide an overview of the pathology of PD and the data supporting the potential neuroprotective capacity of increased polyphenols in the diet. Evidence suggests that the intake of dietary polyphenols may inhibit neurodegeneration and the progression of PD. Polyphenols appear to have a positive effect on the gut microbiome, which may decrease inflammation that contributes to the disease. Therefore, a diet rich in polyphenols may decrease the symptoms and increase quality of life in PD patients.
Highlights
Parkinson’s disease (PD) is a progressive neurodegenerative disorder that is characterized by a loss of dopaminergic neurons, leading to bradykinesia, rigidity, tremor at rest, and postural instability, as well as non-motor symptoms such as olfactory impairment, pain, autonomic dysfunction, impaired sleep, fatigue, and behavioral changes
Neuronal cell death occurs via two mechanisms: Cell-autonomous, where cell death occurs by the accumulation of intrinsic damage of degrading neurons, and non-cell-autonomous, where neuronal degeneration occurs via pathological interaction with glial cells or infiltration of peripheral immune cells [55]
epigallocatechin gallate (EGCG) is the only polyphenol found in the plasma in its free form as other catechins are highly conjugated from Phase II biotransformations, galloylated catechins have not been recovered in urine as they are preferentially excreted in bile [159]
Summary
More than two centuries ago, in 1817, James Parkinson first described the disease with his namesake in his essay, An Essay on the Shaking Palsy [1]. Parkinson’s disease (PD) is a slow progressive neurodegenerative disorder that predominately affects dopaminergic neurons in the substantia nigra pars compacta (SNpc). PD is a debilitating condition caused by a mixture of genetic and environmental factors affecting various neuroanatomical sites and begins years before the diagnosis can be made [2]. The early disease can be divided into three stages: (i) Preclinical PD, the beginning of neurodegenerative processes but lack evident signs or symptoms; (ii) prodromal PD, the presence of signs and symptoms, insufficient to define disease; and (iii) clinical PD, with diagnosis of PD based on the presence of classical motor signs [3]. Non-motor symptoms such as olfactory impairment, pain, autonomic dysfunction (orthostatic hypotension, GI dysfunctions), impaired sleep, fatigue, and behavioral changes (depression, anxiety, apathy) are observed [5]
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