Nutraceuticals: An integrative approach to starve Parkinson’s disease

Abstract

The therapeutic approach of multifactorial complex diseases is always a challenge; Parkinson’s disease (PD) is a heterogeneous neurodegenerative disorder triggered by genetic and environmental factors, contributing to its etiology. Indeed, several pathogenic mechanisms lead to selective dopaminergic neuronal injury, including oxidative stress, mitochondrial dysfunction, alteration of endoplasmic reticulum-to-Golgi protein trafficking, excitotoxicity, and neuroinflammation. Current treatment approaches include mainly dopamine replacement therapy or optimizing dopaminergic transmission; however, these strategies that do not counteract the pathogenic mechanisms underlying PD symptoms and often are less effective over time. Recently, there has been growing interest in the therapeutic use of nutraceuticals, that could represent an integrative approach to the pharmacological standard therapy and specifically affect one or more pathogenic pathways. The intake of nutraceuticals or nutritional modifications are generally safe and can be combined with current common drug therapy in most cases to improve the patient’s quality of life and/or mitigate PD symptoms. The current review focuses on several key nutritional compounds and dietary modifications that are effective on several pathogenic pathways involved in PD onset and progression, and further highlights the rationale behind their potential use for the prevention and treatment of PD.

Apitherapy for Parkinson’s Disease: A Focus on the Effects of Propolis and Royal Jelly

“…PD is a multidimensional condition that results from various factors: heredity, lifestyle, nutritional, hormonal, physical, and psychosocial. Evolving knowledge indicates that PD pathology first occurs in the olfactory mucosa and the gut in response to alterations of gut microbiota as a result of direct exposure to ingested toxins or pathogens [ 6 , 9 ]. α -Synuclein—a major contributor to neuronal death in PD—appears in enteric nerves and enteroendocrine cells of PD patients, which is associated with the occurrence of gastrointestinal (GI) symptoms in 70–80% of patients as early as a decade before motor and neurological signs appear.…”

“…However, it turns to be less effective over time, and it exerts no effect on all nonmotor symptoms. Even more, some of them (e.g., GI symptoms) interfere with the action of the drug and severely alter patients' quality of life [ 6 , 10 ]. Therefore, recent researches have focused on the use of multifunctional, natural agents, and nutritional modifications as safe adjunctive treatments to impede disease progress, alleviate its symptoms, and promote quality of life in PD patients [ 6 , 19 ].…”

“…Experimental models of PD are distinguished into 3 main classes: genetic, pharmacological, and environmental ( Figure 3 ). Various models express PD characteristics only partially, i.e., there is no typical model that perfectly exhibits the typical progressive, behavioral, neurologic, and pathological features of the disease, which may represent a challenge for PD research [ 6 ]. Many transgenic PD mice models have been recently generated by inducing mutations in genes involved in PD pathology such as A53T α -Syn, Thy- α -Syn, and aggregates of α -Syn preformed fibrils (PFF).…”

“…Many transgenic PD mice models have been recently generated by inducing mutations in genes involved in PD pathology such as A53T α -Syn, Thy- α -Syn, and aggregates of α -Syn preformed fibrils (PFF). These mutations accelerate intraneuronal accumulation of α -synuclein in a fashion similar to the naturally occurring ones [ 6 , 77 ]. For instance, A53T α -Syn model develops mid- to late-onset neurodegeneration with aggregation of filamentous α -synuclein cytoplasmic inclusions all over the neuroaxis [ 77 ].…”

“…Parkinson's disease (PD) is an age-related neurological disorder that affects more than 6.3 million people [ 4 , 5 ] accounting for around 2% of the world's population [ 6 ], which makes it the second most prevalent neurodegenerative disease worldwide [ 7 ]. The key pathological hallmark of the disease is chronic, progressive, and selective degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNC) that results from intraneuronal accumulation of misfolded proteins, mainly the synaptic protein α -synuclein, a major component of Lewy bodies [ 4 , 6 , 8 ].…”