Abstract
Neuroinflammation is increasingly recognized as an important pathophysiological feature of neurodegenerative diseases such as Parkinson's disease (PD). Recent evidence suggests that neuroinflammation in PD might originate in the intestine and the bidirectional communication between the central and enteric nervous system, the so-called “gut-brain axis,” has received growing attention due to its contribution to the pathogenesis of neurological disorders. Diet targets mediators of inflammation with various mechanisms and combined with dopaminergic treatment can exert various beneficial effects in PD. Food-based therapies may favorably modulate gut microbiota composition and enhance the intestinal epithelial integrity or decrease the proinflammatory response by direct effects on immune cells. Diets rich in pre- and probiotics, polyunsaturated fatty acids, phenols including flavonoids, and vitamins, such as the Mediterranean diet or a plant-based diet, may attenuate chronic inflammation and positively influence PD symptoms and even progression of the disease. Dietary strategies should be encouraged in the context of a healthy lifestyle with physical activity, which also has neuroimmune-modifying properties. Thus, diet adaptation appears to be an effective additive, nonpharmacological therapeutic strategy that can attenuate the chronic inflammation implicated in PD, potentially slow down degeneration, and thereby modify the course of the disease. PD patients should be highly encouraged to adopt corresponding lifestyle modifications, in order to improve not only PD symptoms, but also general quality of life. Future research should focus on planning larger clinical trials with dietary interventions in PD in order to obtain hard evidence for the hypothesized beneficial effects.
Highlights
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by a loss of dopaminergic neurons in the substantia nigra (SN) as well as nondopaminergic neurons, including cholinergic neurons, norepinephrinergic neurons, serotoninergic neurons, and neurons of the enteric nervous system [1, 2]. e disease is characterized by intracellular inclusions composed of fibrillar alpha-synuclein (a-Syn) and ubiquitinated proteins within neurons in various brain regions [3]
Neuroinflammation is increasingly recognized as an important pathophysiological feature of neurodegenerative diseases such as PD. erefore, there is growing interest in developing therapeutic strategies targeting neuroinflammation in PD
Drugs to treat inflammation, such as NSAIDs, that have been shown to reduce the risk of PD in large epidemiological studies, have adverse effects, cross poorly the blood-brain barrier (BBB), and rather halt the proinflammatory response than induce an “anti-inflammatory” response [11]
Summary
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by a loss of dopaminergic neurons in the substantia nigra (SN) as well as nondopaminergic neurons, including cholinergic neurons, norepinephrinergic neurons, serotoninergic neurons, and neurons of the enteric nervous system [1, 2]. e disease is characterized by intracellular inclusions (so-called Lewy bodies) composed of fibrillar alpha-synuclein (a-Syn) and ubiquitinated proteins within neurons in various brain regions [3]. Dopamine replacement therapy, which remains the main pharmacological treatment in PD, alleviates the motor symptoms of the disease such as rigidity, resting tremor, and bradykinesia, while it influences to a lesser extent the nonmotor symptoms such as autonomic dysfunction, sensory, and neuropsychiatric disorders [13], has side effects, and has no proven effect on slowing down disease progression. For this reason, there is an urgent need to develop new additive therapeutic strategies targeting PD pathogenesis. There is an urgent need to develop new additive therapeutic strategies targeting PD pathogenesis. ere is growing evidence that diet [14, 15] can attenuate the neuroinflammation implicated in the pathophysiology of PD, rendering it an attractive nonpharmacological modulator of chronic inflammation in PD
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