In Vitro and in Vivo Neuroprotective Effects of Walnut (Juglandis Semen) in Models of Parkinson’s Disease

Abstract

Monoamine oxidase (MAO) catalyzes the oxidative deamination of monoamines including dopamine (DA). MAO expression is elevated in Parkinson’s disease (PD). An increase in MAO activity is closely related to age, and this may induce neuronal degeneration in the brain due to oxidative stress. MAO (and particularly monoamine oxidase B (MAO-B)) participates in the generation of reactive oxygen species (ROS), such as hydrogen peroxide that are toxic to dopaminergic cells and their surroundings. Although the polyphenol-rich aqueous walnut extract (JSE; an extract of Juglandis Semen) has been shown to have various beneficial bioactivities, no study has been dedicated to see if JSE is capable to protect dopaminergic neurons against neurotoxic insults in models of PD. In the present study we investigated the neuroprotective potential of JSE against 1-methyl-4-phenylpyridinium (MPP+)- or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicities in primary mesencephalic cells and in a mouse model of PD. Here we show that JSE treatment suppressed ROS and nitric oxide productions triggered by MPP+ in primary mesencephalic cells. JSE also inhibited depletion of striatal DA and its metabolites in vivo that resulted in significant improvement in PD-like movement impairment. Altogether our results indicate that JSE has neuroprotective effects in PD models and may have potential for the prevention or treatment of PD.

Beneficial Effects of Walnuts on Cognition and Brain Health

“…PD is characterized by the progressive loss of dopaminergic neurons and by clinical symptoms, including movement impairment, postural imbalance, tremor, and rigidity. In a mouse model of PD, walnut extract improved symptoms of PD (postural balance, motor coordination, and movement), reduced oxidative stress, and protected neurons [39].…”

Batryticatus Bombyx Protects Dopaminergic Neurons against MPTP-Induced Neurotoxicity by Inhibiting Oxidative Damage

“…Decreased dopamine contents are associated with adverse movement impairments, including bradykinesia, resting tremor, and postural instability [1,2]. Although the plausible mechanism of PD is unknown, neuronal oxidation, neuroinflammation, and consequent mitochondria-mediated neuronal damage have been implicated in PD pathogenesis [1,3]. Dopaminergic neurons are rich in reactive oxygen species (ROS), which are a major cause of PD due to oxidative stress.…”

“…ROS is one of the factors that reduces cognitive and motor performance in neurodegenerative diseases. Oxidative stress is associated with a decline in oxidative defense mechanisms mediated by catalase (CAT) and glutathione (GSH), and increased oxidative damage involving hydroxyl radicals and peroxynitrite levels [3,4]. Furthermore, ROS accumulation in PD may be increased by exposure to pesticides and neurotoxins [2,4].…”

A New Perspective on Parkinson’s Disease: Pathology Begins in the Gastrointestinal Tract

“…PD is a chronic disorder, characterized primarily by motor deficits including resting tremor, rigidity, bradykinesia, and postural instability (Burke & O'Malley, 2013;Choi et al, 2016;Lohr & Miller, 2014;Miller et al, 1999;Taylor et al, 2014). Although dopaminergic atrophy in the substantia nigra pars compacta mediates the presence of these motor deficits, the clinical indicators do not appear until over 70% of dopamine (DA) nerve terminals in the striatum have atrophied, suggesting the presence of compensatory mechanisms (Bezard et al, 2013).…”