fps-zm1 has been researched along with Cognition-Disorders* in 2 studies
2 other study(ies) available for fps-zm1 and Cognition-Disorders
| Article | Year |
|---|---|
Targeted inhibition of RAGE reduces amyloid-β influx across the blood-brain barrier and improves cognitive deficits in db/db mice.
To investigate restorative effects of the receptor for advanced glycation end products (RAGE)-specific inhibitor FPS-ZM1 on abnormal amyloid β (Aβ) influx across the blood brain-barrier (BBB) and cognitive deficits in db/db mice.. Aβ influx across the BBB was determined by intra-arterial infusion of. Downregulation of abnormal Aβ influx across the BBB by FPS-ZM1 at higher dosage contributes to reduced neuronal apoptosis, improved hippocampal plasticity and cognitive impairment in db/db mice. Topics: Amyloid beta-Peptides; Animals; bcl-2-Associated X Protein; Benzamides; Blood-Brain Barrier; Brain; Caspase 3; Cognition Disorders; Diabetes Mellitus, Type 2; Disease Models, Animal; Exploratory Behavior; Male; Maze Learning; Mice; Microvessels; Peptide Fragments; Proto-Oncogene Proteins c-bcl-2; Receptor for Advanced Glycation End Products; Receptors, Leptin; Synaptic Transmission | 2018 |
Effects of RAGE-Specific Inhibitor FPS-ZM1 on Amyloid-β Metabolism and AGEs-Induced Inflammation and Oxidative Stress in Rat Hippocampus.
An increased level of advanced glycation end products (AGEs) is observed in brains of patients with Alzheimer's disease (AD). AGEs and receptor for AGEs (RAGE) play important roles in the pathogenesis of AD. FPS-ZM1 is a high-affinity RAGE-specific blocker that inhibits amyloid-β binding to RAGE, neurological damage and inflammation in the APP(sw/0) transgenic mouse model of AD. FPS-ZM1 is not toxic to mice and can easily cross the blood-brain barrier. In this study, an AGEs-RAGE-activated rat model were established by intrahippocampal injection of AGEs, then these rats were treated with intraperitoneal administration of FPS-ZM1 and the possible neuroprotective effects were investigated. We found that AGEs administration induced an-regulation of Abeta production, inflammation, and oxidative stress, and an increased escape latency of rats in the Morris water maze test, all of these are significantly reduced by FPS-ZM1 treatment. Our results suggest that the AGEs-RAGE pathway is responsible for cognitive deficits, and therefore may be a potential treatment target. FPS-ZM1 might be a novel therapeutic agent to treat AD patients. Topics: Amyloid beta-Peptides; Animals; Antioxidants; Benzamides; Cognition Disorders; Cytokines; Glycation End Products, Advanced; Hippocampus; Inflammation; Male; Maze Learning; Memory; Neuroprotective Agents; Oxidative Stress; Peptide Fragments; Rats, Wistar; Receptor for Advanced Glycation End Products | 2016 |