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Pharmacological Management of Alzheimer’s Disease
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Rakesh Kumar, Rajan Kumar, Abhinav Anand, Neha Sharma, Navneet Khurana
It is developed as a potential cognition enhancer and 5-HT6 receptor antagonist. Blockade of the 5-HT6 receptor is found to improve the cognitive function. Cognitive dysfunction is recognized as a key symptom of the AD; SB-271046 can be useful as therapeutic potential in the treatment of the AD. In various research articles, it has been found to improve cognitive function. Still, there is a lack of facts availability regarding SB-271046 (Upton et al., 2008).
Neuropsychology of Cognitive Aging in Rodents
Published in David R. Riddle, Brain Aging, 2007
Joshua S. Rodefer, Mark G. Baxter
Administration of the 5-HT(6) receptor antagonist SB-271046 improved acquisition and consolidation in a water maze task in aged rats. Treatment with SB-271046 improved swim strategy, escape latencies, and task recall, suggesting that the drug may enhance cognitive processes as well as ameliorate age-related cognitive deficits observed in older animals [78]. In addition, Froestl et al. [79] examined the effects of the novel GABA(B) receptor antagonist SGS742. Chronic administration of SGS742 was reported to upregulate GABA(B) receptors in the frontal cortex of rats and produce cognitive enhancing effects in aged rats in both radial and water maze tasks.
The role of 5 HT6-receptor antagonists in Alzheimer’s disease: an update
Published in Expert Opinion on Investigational Drugs, 2018
Rita Khoury, Noam Grysman, Jake Gold, Kush Patel, George T. Grossberg
Thus, 5-HT6 receptors are primarily theorized to regulate the balance between excitatory and inhibitory signaling, through the modulation of GABA and glutamate levels. In one study, activation of the 5-HT6 receptor, after administration of a selective experimental 5-HT6 receptor agonist (WAY-181187) has been shown to enhance extracellular GABA concentrations in the rat cortex, without affecting other neurotransmitters’ concentrations such as glutamate, serotonin, norepinephrine or dopamine [21]. In another study, administration of 5-HT6 receptor antagonists such as SB-271046 was shown to produce significant 2- and 3- fold increases in the extracellular concentrations of glutamate, in the hippocampus and frontal cortex, which were not reversed by atropine administration, demonstrating that enhanced excitatory neurotransmission wasn’t the result of enhanced cholinergic neurotransmission with this compound [22].