lncRNA CTBP1-AS2 promotes proliferation and migration of glioma by modulating miR-370-3p-Wnt7a-mediated epithelial-mesenchymal transition.

Glioma is one of the most common and aggressive malignant primary brain tumors, with a poor 5-year survival rate. The long noncoding RNA (lncRNA) CTBP1-AS2 has been shown to be correlated with the prognosis of cancer, but the role of CTBP1-AS2 in glioma and its concrete mechanism is fully unknown. The clinical data and tissues of glioma patients were analyzed.

RTP801/REDD1 regulates the timing of cortical neurogenesis and neuron migration.

The generation, differentiation, and migration of newborn neurons are critical features of normal brain development that are subject to both extracellular and intracellular regulation. However, the means of such control are only partially understood. Here, we show that expression of RTP801/REDD1, an inhibitor of mTOR (mammalian target of rapamycin) activation, is regulated during neuronal differentiation and that RTP801 functions to influence the timing of both neurogenesis and neuron migration.

(99m)Tc hexamethyl-propylene-aminoxime single-photon emission computed tomography prediction of conversion from mild cognitive impairment to Alzheimer disease.

Objective: To examine the utility of single-photon emission computed tomography (SPECT) to predict conversion from mild cognitive impairment (MCI) to Alzheimer disease (AD).

Design: Longitudinal, prospective study.

Setting: University-based memory disorders clinic.

Rapamycin protects against neuron death in in vitro and in vivo models of Parkinson's disease.

We report that rapamycin, an allosteric inhibitor of certain but not all actions of the key cellular kinase mammalian target of rapamycin (mTOR), protects neurons from death in both cellular and animal toxin models of Parkinson's disease (PD). This protective action appears to be attributable to blocked translation of RTP801/REDD1/Ddit4, a protein that is induced in cell and animal models of PD and in affected neurons of PD patients and that causes neuron death by leading to dephosphorylation of the survival kinase Akt. In support of this mechanism, in PD models, rapamycin spares phosphorylation of Akt at a site critical for maintenance of its survival-promoting activity.

RTP801 is induced in Parkinson's disease and mediates neuron death by inhibiting Akt phosphorylation/activation.

Previously, we reported that RTP801, a stress regulated protein, is induced in multiple cellular models of Parkinson's disease (PD), in an animal model of PD and in dopaminergic neurons of PD patients. In cellular PD models, RTP801 is both sufficient and necessary for death. We further showed that RTP801 and PD mimetics such as 6-OHDA trigger neuron death by suppressing activation of the key kinase mammalian target of rapamycin (mTOR).