Colivelin ameliorates amyloid β peptide-induced impairments in spatial memory, synaptic plasticity, and calcium homeostasis in rats. Hippocampus 2015 Mar;25(3):363-72
Date
10/22/2014Pubmed ID
25332198DOI
10.1002/hipo.22378Scopus ID
2-s2.0-84922629412 (requires institutional sign-in at Scopus site) 21 CitationsAbstract
Amyloid β peptide (Aβ) has been thought to be neurotoxic and responsible for the impairment of learning and memory in Alzheimer's disease (AD). Humanin (HN), a 24 amino acid polypeptide first identified from the unaffected occipital lobe of an AD patient, is believed to be neuroprotective against the AD-related neurotoxicity. In this study, we investigated the neuroprotective effects of Colivelin (CLN), a novel HN derivative, against Aβ by using behavioral test, in vivo electrophysiological recording, and intracellular calcium imaging. Our results showed that intrahippocampal injection of CLN (0.2 nmol) effectively prevented Aβ25-35 (4 nmol)-induced deficits in spatial learning and memory of rats in Morris water maze test; the suppression of in vivo hippocampal long term potentiation (LTP) by Aβ25-35 was nearly completely prevented by CLN; in addition, CLN pretreatment also effectively inhibited Aβ25-35-induced calcium overload in primary cultured hippocampal neurons. These results indicate that CLN has significant neuroprotective properties against Aβ, and CLN may holds great promise for the treatment and prevention of AD.
Author List
Wu MN, Zhou LW, Wang ZJ, Han WN, Zhang J, Liu XJ, Tong JQ, Qi JSAuthor
Jiaqing Tong PhD Postdoctoral Researcher 3 in the Neurology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Amyloid beta-PeptidesAnimals
Calcium
Cells, Cultured
Hippocampus
Homeostasis
Intracellular Signaling Peptides and Proteins
Long-Term Potentiation
Maze Learning
Memory Disorders
Neuronal Plasticity
Neurons
Peptide Fragments
Rats
Rats, Sprague-Dawley
