Background and Objectives. The exact pathological mechanism of Parkinson’s disease (PD) remains elusive, and the existing therapies fail to reverse the disease progression. This study intended to explore the epigenetic anti-inflammatory mechanism of ketogenic diet (KD). Materials and Methods. The neuroprotective effect of ketosis state prior to the onset of PD (preventive KD, KDp) was compared with that receiving KD after the onset (therapeutic KD, KDt) in the lipopolysaccharide- (LPS-) induced rat PD model. A total of 100 rats were randomly assigned to the following 4 groups: sham, LPS, LPS + KDp, and LPS + KDt groups. Results. Significant dopamine deficient behaviors (rotational behavior and contralateral forelimb akinesia), upregulation of proinflammatory mediators (TNF-α, IL-1β, and IL-6), loss of dopaminergic neurons, reduction of mGluR5+ microglia cells, increase of TSPO+ microglia cells, reduction of H3K9 acetylation in the mGluR5 promoter region and mGluR5 mRNA expression, and decline in the phosphorylation levels of Akt/GSK-3β/CREB pathway were observed after the intervention of LPS ( P < 0.01 ). TSPO and DAT PET imaging revealed the increased uptake of 18F-DPA-714 in substantia nigra and decreased uptake of 18F-FP-CIT in substantia nigra and striatum in LPS-treated rats ( P < 0.001 ). These impairments were alleviated by the dietary intervention of KD, especially with the strategy of KDp ( P < 0.05 ). Conclusions. The anti-inflammatory effect of KD on PD was supposed to be related to the modulation of Akt/GSK-3β/CREB signaling pathway mediated by the histone acetylation of mGluR5 promotor region. The KD intervention should be initiated prior to the PD onset in high-risk population to achieve a more favorable outcome.

No abstract

The aim of this study was to explore the influences of age‐matched control and/or age‐specific template on voxel‐wise analysis of brain 18 F‐fluorodeoxyglucose positron emission tomography ( 18 F‐FDG PET) data in pediatric epilepsy patients. We, retrospectively, included 538 pediatric (196 females; age range of 12 months to 18 years) and 35 adult subjects (18 females; age range of 20–50 years) without any cerebral pathology as pediatric and adult control group, respectively, as well as 109 pediatric patients with drug‐resistant epilepsy (38 females; age range of 13 months to 18 years) as epilepsy group. Statistical parametric mapping (SPM) analysis for 18 F‐FDG PET data of each epilepsy patients was performed in four types of procedures, by using age‐matched controls with age‐specific template, age‐matched controls with adult template, adult controls with age‐specific template or adult controls with adult template. The numbers of brain regions affected by artifacts among these four types of SPM analysis procedures were further compared. Any template being adopted, the artifacts were significantly less in SPM analysis procedures using age‐matched controls than those using adult controls in each age range ( p < .001 in each comparison), except in the age range of 15–18 ( p > .05 in each comparison). No significant difference was found in artifacts, when compared procedures using the identical control group with different templates ( p = 1.000 in each comparison). In conclusion, the age stratification for age‐matched control should be divided as many layers as possible for the SPM analysis of brain 18 F‐FDG PET images, especially in pediatric patients ≤14‐year‐old, while age‐specific template is not mandatory.

No abstract

No abstract