Calorie restriction is known to suppress inflammation to some degree, alongside many other benefits to health that result from the reaction of cells and biological systems to a reduced calorie intake. Since chronic inflammation in brain tissue is implicated in the onset and development of neurodegenerative conditions, this makes calorie restriction a topic of interest in this part of the field. With a few exceptions, that interest largely manifests as research aimed at reproducing some of the metabolic alterations of calorie restriction with small molecule drugs, however, rather than more more rigorously testing calorie restriction as a therapy.
Parkinson’s disease (PD) is the second most common neurodegenerative disease. To date, PD is still incurable and its pathogenesis remains elusive. Evidence from experimental studies reveals that mechanisms including protein misfolding and aggregation, neuroinflammation, mitochondrial dysfunction, and altered gut bacteria composition contribute to PD development. As of now, a number of medication strategies have been widely applied to control the motor and non-motor symptoms of PD and improve the quality of life. However, with long-term application of these drugs and as the disease progresses, adverse effects emerge. Moreover, these medications could neither effectively prevent the disease onset nor stop the disease progression. Recently, lifestyle interventions in the promotion of healthy brain aging and the prevention and treatment of central nervous system (CNS) diseases have risen into the spotlight, which could be promisingly complementary to the conventional PD pharmacotherapy.
Dietary restriction (DR), which involves a moderate reduction in food intake while avoiding malnutrition, has been proven to be effective in holding back aging and relieving age-related chronic diseases, including cancer, cardiovascular disease, diabetes, and neurodegenerative disorders. The beneficial actions of DR involve metabolic, hormonal, and immunomodulatory mechanisms. DR could reduce obesity and visceral fat, thus preventing metabolic risk factors. It increases insulin sensitivity, glucose tolerance, and ghrelin level. It can also induce adipose tissue transcriptional reprogramming, involving ways to regulate mitochondrial bioenergy, anti-inflammatory response, and longevity. Moreover, a potential role of DR in regulating the gut-brain axis has been well described in diseases of CNS and intestinal microbiota transplantation has been shown to be effective in Alzheimer’s disease (AD) and multiple sclerosis (MS). Here, we summarize the strategies of DR from clinical and laboratory studies, and review the current findings of DR in preventing and ameliorating PD, with an emphasis on the possible mechanisms.