Impairments in systematic and regional glucose metabolism exist in patients with Parkinson's disease (PD) at every stage of the disease course, and such impairments are associated with the incidence, progression, and special phenotypes of PD, which affect each physiological process of glucose metabolism including glucose uptake, glycolysis, tricarboxylic acid cycle, oxidative phosphorylation, and pentose phosphate shunt pathway. These impairments may be attributed to various mechanisms, such as insulin resistance, oxidative stress, abnormal glycated modification, blood-brain-barrier dysfunction, and hyperglycemia-induced damages. These mechanisms could subsequently cause excessive methylglyoxal and reactive oxygen species production, neuroinflammation, abnormal aggregation of protein, mitochondrial dysfunction, and decreased dopamine, and finally result in energy supply insufficiency, neurotransmitter dysregulation, aggregation and phosphorylation of α-synuclein, and dopaminergic neuron loss. This review discusses the glucose metabolism impairment in PD and its pathophysiological mechanisms, and briefly summarized the currently-available therapies targeting glucose metabolism impairment in PD, including glucagon-likepeptide-1 (GLP-1) receptor agonists and dual GLP-1/gastric inhibitory peptide receptor agonists, metformin, and thiazoledinediones.

Aims: Recent studies showed that patients with various bacterial, viral, and fungal infections might be at increased risk of Parkinson's disease (PD). However, the risk of PD in patients with each specific infection varied. This meta‐analysis estimated the association between various infections and PD risk.Methods: Literature published from January 1965 to October 2019 in PubMed and EMBASE databases was searched. Data were extracted and pooled using random/fixed effects model. Sensitivity analysis and meta‐regression were also performed to analyze the source of heterogeneity. Publication bias was estimated by the trim and fill.Results: Twenty‐three out of 6,609 studies were included. Helicobacter pylori (HP; pooled OR = 1.653, 1.426–1.915, p < .001), hepatitis C virus (HCV; pooled OR = 1.195, 1.012–1.410, p = .035), Malassezia (pooled OR = 1.694, 1.367–2.100, p < .001), and pneumoniae (pooled OR = 1.595, 1.020–2.493, p = .041) infection were associated with increased PD risk. Influenza virus, herpes virus, hepatitis B virus, scarlet fever, mumps virus, chicken pox, pertussis, German measles, and measles were not associated with PD risk. After antiviral treatment against HCV reduced the risk of PD in patients with HCV infection (OR = 0.672, 0.571–0.791, p < .001). Significant heterogeneity exists among the included studies.Conclusion: Patients with infection of HP, HCV, Malassezia, pneumoniae might be an increased risk of PD. Antiviral treatment of HCV could reduce the risk of PD.

Tremor is one of the core symptoms of Parkinson’s disease (PD), but its mechanism is poorly understood. The cerebellum is a growing focus in PD-related researches and is reported to play an important role in tremor in PD. The cerebellum may participate in the modulation of tremor amplitude via cerebello-thalamo-cortical circuits. The cerebellar excitatory projections to the ventral intermediate nucleus of the thalamus may be enhanced due to PD-related changes, including dopaminergic/non-dopaminergic system abnormality, white matter damage, and deep nuclei impairment, which may contribute to dysregulation and resistance to levodopa of tremor. This review summarized the pathological, structural, and functional changes of the cerebellum in PD and discussed the role of the cerebellum in PD-related tremor, aiming to provide an overview of the cerebellum-related mechanism of tremor in PD.