Identification of metabolite biomarkers for L-DOPA-induced dyskinesia in a rat model of Parkinson's disease by metabolomic technology.

L-DOPA-induced dyskinesia (LID) is a frequent complication of chronic L-DOPA therapy in the clinical treatment of Parkinson's disease (PD). The pathogenesis of LID involves complex molecular mechanisms in the striatum. Metabolomics can shed light on striatal metabolic alterations in LID.

Exendin-4, a glucagon-like peptide 1 receptor agonist, protects against amyloid-β peptide-induced impairment of spatial learning and memory in rats.

Type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) share specific molecular mechanisms, and agents with proven efficacy in one may be useful against the other. The glucagon-like peptide-1 (GLP-1) receptor agonist exendin-4 has similar properties to GLP-1 and is currently in clinical use for T2DM treatment. Thus, this study was designed to characterize the effects of exendin-4 on the impairment of learning and memory induced by amyloid protein (Aβ) and its probable molecular underlying mechanisms.

Down-regulation of Homer1b/c protects against chemically induced seizures through inhibition of mTOR signaling.

Background: Homer is a family of post synaptic density proteins functionally and physically attached to target proteins at proline-rich sequences. Reducing Homer1b/c expression has been shown in previous studies to be protective against excitotoxic insults, implicating Homer1b/c in the physiological regulation of aberrant neuronal excitability.

Methods: To test the efficacy of a Homer1b/c reducing therapy for disorders with a detrimental hyperexcitability profile in mice, we used small interfere RNA (siRNA) to decrease endogenous Homer1b/c expression in mouse hippocampus.

Dynamin-related protein 1 inhibitors protect against ischemic toxicity through attenuating mitochondrial Ca2+ uptake from endoplasmic reticulum store in PC12 cells.

Intracellular calcium homeostasis disorder and mitochondrial dysfunction are involved in many acute and chronic brain diseases, including ischemic brain injury. An imbalance in mitochondrial fission and fusion is one of the most important structural abnormalities found in a large number of mitochondrial dysfunction related diseases. Here, we investigated the effects of mitochondrial division inhibitor A (mdivi A) and mdivi B, two small molecule inhibitors of mitochondrial fission protein dunamin-related protein 1 (Drp-1), in neuronal injury induced by oxygen-glucose deprivation (OGD) in PC12 cells.

[Diffusion characteristics of subcortical structures in patients with subcortical ischemic vascular disease and its correlation to cognitive function].

Objective: To explore the diffusion-tensor imaging (DTI) characteristics of normal-appearing white matter (NAWM) and normal-appearing gray matter (NAGM) on conventional magnetic resonance imaging (MRI) in patients with subcortical ischemic vascular disease (SIVD) and examine the relation of such features with the general cognitive function of the patients.

Methods: DTI was performed in 46 SIVD patients and 34 age-matched control subjects with normal MRI findings. The apprarent diffusion coeeficient (ADC) and fractional anisotropy (FA) were measured within the regions of white matter lesions (WMLs), NAWM and NAGM.

[Effect of Shuanghuanglian injection on cerebral nuclear factor-kappaB expression in mice with viral encephalitis].

Objective: To observe the effect of Shuanghuanglian injection on cerebral expression of nuclear factor-kappaB (NF-kappaB) in mice with viral encephalitis.

Methods: The mice with experimental viral encephalitis received treatment with Shuanghuanglian injection at the dose of 0.2, 1.