The potential approaches to treating neonatal H-I injury are as follows: 1. Inhibiting M1 microglia to secrete pro-inflammatory cytokines or to promote microglia M2 polarization. 2. Targeting OPCs and oligodendrocytes and promoting their differentiation and maturation to maintain axonal integrity and conductivity and restoring axonal functions through remyelination.

Oligodendrocyte progenitor cells cannot extend cellular process in the presence of Chondroitin Sulfate Proteoglycans. Treatment of OPCs with different neurotrophic factors (BDNF, GDNF, and NT-3) allows OPCs to overcome the inhibitory effects of CSPGs, allowing for OPC process outgrowth which is a critical step in the differentiation of OPCs.

Glial cell line-derived neurotrophic factor derived from glioma cells upregulate matrix metallopeptidase 9 and 14 expression on microglia, which in turn promote glioma progression.

Genetic ablation of G protein-coupled receptor 37-like 1 results in increased patched 1 expression and internalization. This leads to the intracellular accumulation of cholesterol, with concomitant stimulation of sonic hedgehog (Shh) production and activation of Shh-induced proliferative signaling.

d-glucose uptake in astrocytes is an essential source for the noradrenaline-induced increase in intracellular L-lactate. We found that intracellular l-lactate arises exclusively from the glycogen—a temporary energy store in the brain. The glycolytic pathway intermediates also support oxidative phosphorylation in mitochondria. At rest, a large proportion of d-glucose is metabolized in the Krebs cycle, since the resting l-lactate concentration is low. This is increased when the Krebs cycle is blocked or when cells are stimulated with noradrenaline.

By observing the behavior of mice in their home cage environment, using the powerful PhenoTyper tracking system, we demonstrate that mice display dramatic reductions in movement and exploration when isolated from their cage mates, an instantaneous effect that escalates over the next 5 days, which is reversible upon re-pairing.

The brain activity of the four brain regions during visuo-guided grip force tracking tasks were detected by functional near-infrared spectroscopy. Pearson's correlation method, partial correlation method, and a pairwise maximum entropy model were used to get a more comprehensive and accurate functional connectivity for precise grip force control.

Oxidative stress implicates mitochondrial damage and effects on mitochondrial function, production of ATP, mitochondrial dynamics and biogenesis. The mitochondrial dysfunction eventually demonstrates its lethal behaviour on Aβ clearance and mitochondrial fission, especially on the protein Drp1. In AD pathogenesis, Drp1 can play an important regulatory role in mitophagy and autophagy. The miR-499 causes suppression of calcineurin-mediated dephosphorylation of Drp1, whereas miR-30a inhibits mitochondrial fission by suppressing p53 and subsequent Drp-1 downstream signaling. Mitochondrial targeted antioxidant (MTA) molecules such as Mdivi1, SS31 and Dynasore can reduce excessive mitochondrial fission activity of Drp1 and restore normal mitochondrial functions, fusion-fission activities, mitophagy and autophagy functions in clearing dead mitochondria for normal synaptic functions.

In similarly aged individuals, traumatic brain injury (TBI) induced more profound sleep alterations than Alzheimer's disease (AD), with incongruous inflammation. Altered sleep may be associated with deleterious pathological processes and unique pathological sleep pathways may exist in older individuals that incur TBI compared with similarly aged individuals that have AD.

The protein α-synuclein is central to Parkinson's disease. For the first time, we report that α-synuclein from Parkinson's patients brain samples caused signaling deficits in brain cells, and novel drug candidates known to block the sigma-2 receptor complex reversed these deficits.

This PET study characterized D2 receptor (D2R) availability within extra-striatal regions in Parkinson's disease (PD) patients with (+) and without (−) REM sleep behavior disorder (RBD). With disease progression, only PD-RBD+ patients showed steep decline in D2R availability within the left uncus parahippocampus. Beyond the striatum, extra-striatal dopaminergic system may also contribute to PD-RBD in advanced stages.