Combination of Aβ clearance and neurotrophic factors as a potential treatment for Alzheimer's disease.

There is no effective drug to treat Alzheimer's disease (AD), a neurodegenerative disease affecting an estimated 30 million people around the world. Strongly supported by preclinical and clinical studies, amyloid-beta (Aβ) may be a target for developing drugs against AD. Meanwhile, the fact that localized neuronal death/loss and synaptic impairment occur in AD should also be considered.

Schizandrin prevents dexamethasone-induced cognitive deficits.

Objective: To model glucocorticoid-induced cognitive impairment and evaluate the neuroprotection by schizandrin (Sch) against dexamethasone (Dex)-induced neurotoxicity in vivo and in vitro.

Methods: Cerebral cortical cells from neonatal Sprague-Dawley rats (within 24 hours after birth) were cultured for 9 days, and then treated with Dex (10(-4), 10(-5), 10(-6) or 10(-7) mol/L) for 24 h or pretreated with 10(-4) mol/L Dex for 24 h followed by 10, 20, 40, or 80 μmol/L Sch for 48 h. Cell viability was assessed using the MTT assay.

Phosphorylation of Akt is involved in protocatechuic acid-induced neurotrophic activity.

Objective: To investigate the mechanisms underlying protocatechuic acid (PCA)-induced neurotrophic effects on cultured cortical neurons.

Methods: The mRNA expression of microtubule-associated protein 2 (MAP2) and brain-derived neurotrophic factor (BDNF) were measured by real-time quantitative PCR (qPCR). Subsequently, antagonists were used to study the signaling pathways activated by PCA and western blotting was used to detect the phosphorylation level of kinase-related protein.

Daphnetin prevents chronic unpredictable stress-induced cognitive deficits.

Chronic exposure to stress hormones might impair cognitive functions such as learning and memory, which were associated with many mood disorders and neurodegenerative diseases. In this study, we aimed to screen for effective compounds to prevent cognitive deficits induced by chronic stress. Daphnetin was found to protect the cortical neurons against dexamethasone-induced reduction of cell viability in a dose-dependent manner in vitro.

Neurotrophic effects of magnesium fructose 1, 6-diphosphate on cortical neurons.

In this study, we evaluated the neurotrophic effects of magnesium fructose 1, 6-diphosphate (FDP-Mg) on cortical neurons. The results demonstrated that FDP-Mg promoted dendrite outgrowth and neuronal survival in a dose-dependent manner. In order to investigate the associated mechanisms, we determined adenosine triphosphate (ATP) levels and brain-derived neurotrophic factor (BDNF) mRNA expression in cortical neurons.