Geniposide effectively reverses cognitive impairment and inhibits pathological cerebral damage by regulating the mTOR Signal pathway in APP∕PS1 mice.

Objective: The aim of this study is to investigate the protective effects as well as the underlying molecular mechanisms of geniposide in APP/PS1 transgenic mice.

Method: APP/PS1 mice were subjected to intragastric administration of geniposide (50 mg/kg/d) for 8 weeks (including a 2-week behavior test). The novel object recognition (NOR) and the Morris water maze (MWM) tests were used for behavioral assessments.

Neuroprotective role of (Val(8))GLP-1-Glu-PAL in an in vitro model of Parkinson's disease.

The growth factor glucagon-like peptide-1 (GLP-1) is neuroprotective in several animal models of neurodegeneration. Here, we analyzed the neuroprotective effects of a novel protease-resistant GLP-1 analogue, (Val(8))GLP-1-Glu-PAL, which has advantages over older analogues, such as improvement of hippocampal neurogenesis, glucose homeostasis, and insulin secretion. We established an in vitro model of Parkinson's disease using the mitochondrial stressor rotenone in primary cultured mouse neurons pretreated with (Val(8))GLP-1-Glu-PAL.

Geniposide prevents rotenone-induced apoptosis in primary cultured neurons.

Geniposide, a monomer extracted from gardenia and widely used in Chinese medicine, is a novel agonist at the glucagon-like peptide-1 receptor. This receptor is involved in neuroprotection. In the present study, we sought to identify an anti-apoptotic mechanism for the treatment of neurodegenerative diseases.

(Val⁸) glucagon-like peptide-1 prevents tau hyperphosphorylation, impairment of spatial learning and ultra-structural cellular damage induced by streptozotocin in rat brains.

It has being shown that glucagon-like peptide-1 (GLP-1), a new anti-diabetes agent, significantly attenuated beta-amyloid (Aβ) levels in rats. In the present study, (Val(8))GLP-1 was used to prevent impairments in memory formation, tau hyperphosphorylation and ultra-structural changes induced by streptozotocin intracerebroventricular (i.c.

Hepcidin treatment modulates the expression of divalent metal transporter-1, ceruloplasmin, and ferroportin-1 in the rat cerebral cortex and hippocampus.

Elevated iron levels are considered to play a role in the neurodegenerative mechanisms that underlie Alzheimer's and Parkinson's disease. The linkage between hepcidin (Hepc) and ferroportin-1 (FPN1), the divalent metal transporter 1 (DMT1), and ceruloplasmin (CP) in the brain is unknown. To discern the role of Hepc in regulating the expression of these proteins, we investigated FPN1, DMT1, and CP protein and mRNA expression in the brain after the intracerebroventricular injection of Hepc.

Quantitative analysis of iron concentration and expression of ferroportin 1 in the cortex and hippocampus of rats induced by cerebral ischemia.

Iron overload induced by brain ischemia has been shown to be involved in neurodegenerative disease. Little is known about the relationship between brain ischemia and ferroportin 1 (FP1). The aims of this study are: (i) to determine whether iron accumulation in the brain is induced by cerebral hypoperfusion; and (ii) to test whether expression of FP1 is influenced by cerebral ischemia.