Abstract
Parkinson’s Disease (PD) is a neurological disease characterized by the progressive degeneration of the nigrostriatal dopaminergic pathway with consequent loss of neurons in the substantia nigra pars compacta and dopamine depletion. The cytoplasmic inclusions of α-synuclein (α-Syn), known as Lewy bodies, are the cytologic hallmark of PD. The presence of α-Syn aggregates causes mitochondrial degeneration, responsible for the increase in oxidative stress and consequent neurodegeneration. PD is a progressive disease that shows a complicated pathogenesis. The current therapies are used to alleviate the symptoms of the disease without changing its clinical course. Recently, phytocompounds with neuroprotective effects and antioxidant properties such as caffeine have aroused the interest of researchers. The purpose of this review is to summarize the preclinical studies present in the literature and clinical trials recorded in ClinicalTrial.gov, aimed at illustrating the effects of caffeine used as a nutraceutical compound combined with the current PD therapies. Therefore, the preventive effects of caffeine in the neurodegeneration of dopaminergic neurons encourage the use of this alkaloid as a supplement to reduce the progress of the PD.
Highlights
Parkinson’s Disease (PD) is a neurodegenerative disorder characterized by the progressive neurodegeneration of the dopaminergic neurons in the substantia nigra pars compacta and in the corpus striatum [1]
The purpose of this review was to provide an overview of the experimental and clinical studies that described the protective effects of caffeine consumption in the PD
The most common PD animal models involve the use of neurotoxins such as MPTP and 6-OHDA, which induce the selective destruction of the dopaminergic pathways by reproducing the specific characteristics of PD in rodents
Summary
PD is a neurodegenerative disorder characterized by the progressive neurodegeneration of the dopaminergic neurons in the substantia nigra pars compacta and in the corpus striatum [1]. The familial forms of PD are caused by autosomal dominant and recessive mutations in several genes such as α-Syn (SNCA), ubiquitin C-terminal hydrolase L1 (UCHL-1), phosphatase and tensin homolog-induced putative kinase 1 (PINK1), PARKIN (PRKN), protein deglycase (DJ-1) and leucine-rich repeat kinase 2 (LRRK2) [4]. Environmental factors such as exposure to herbicides; heavy metals; and pesticides including rotenone (ROT), dichlorodiphenyltrichloroethane, paraquat (PQ) and maneb (MB) are risk factors for the onset of idiopathic forms of PD [5]
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