Colivelin ameliorates amyloid β peptide-induced impairments in spatial memory, synaptic plasticity, and calcium homeostasis in rats.
Wu. Mei-Na MN; Zhou. Li-Wei LW; Wang. Zhao-Jun ZJ; Han. Wei-Na WN; Zhang. Jun J; Liu. Xiao-Jie XJ; Tong. Jia-Qing JQ; Qi. Jin-Shun JS
Key Findings
- Colivelin injected into rat hippocampus blocked amyloid‑beta‑induced memory loss in the Morris water maze
- It preserved long‑term potentiation, a measure of synaptic plasticity, that amyloid‑beta normally suppresses
- Colivelin prevented calcium overload in cultured hippocampal neurons caused by amyloid‑beta
Practical Outcomes
- The main takeaway is that humanin‑derived Colivelin has strong neuroprotective effects in animal models, hinting at future cognitive‑support or anti‑Alzheimer uses. However, it currently requires invasive brain injection and lacks human dosing data, so there’s no actionable protocol for biohackers now, but it’s worth monitoring for upcoming oral or injectable versions.
Summary
A lab study found that a humanin‑based peptide called Colivelin, when directly injected into the rat brain, stopped the memory‑damaging effects of an Alzheimer‑linked protein, kept brain cells’ communication strong, and prevented harmful calcium buildup. This shows the peptide can protect brain function in animals, but the method isn’t ready for people yet.
Abstract
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.
Study Information
pubmed
2014
2014-10-30T00:00:00.000Z
10.1002/hipo.22378
20
62