Peptide Found in Sea Anemones Might Give Rise to Alzheimer’s Treatment, Study Says

Peptide Found in Sea Anemones Might Give Rise to Alzheimer’s Treatment, Study Says
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Small proteins found in sea anemones can protect nerve cells from the toxic effects of beta-amyloid, a hallmark of Alzheimer’s, and may one day point to a way of treating this disease, a study reports.

The research, “A New Iq-Peptide of the Kunitz Type from the Heteractis magnifica Sea Anemone Exhibits Neuroprotective Activity in a Model of Alzheimer’s Disease,” was published in the Russian Journal of Bioorganic Chemistry.

During a scientific marine expedition to the Seychelles, Far Eastern Federal University (FEFU) researchers collected a tropical sea anemone called Heteractis magnifica. This animal contained a newly identified group of Kunitz-type peptides in its tentacles. Peptides are short chains of amino acids, the building blocks of proteins, and Kunitz-type peptides are protease inhibitors, which means they block the work of enzymes that break up proteins.

Using the structure of the gene coding one of such peptides, researchers synthesized the HMIQ3c1 peptide in a bacterial system (Escherichia coli) that is genetically similar (an analog) to the newly found peptide.

Protease inhibitors used in science have been found in many marine invertebrates and mammals, including sea anemones. Kunitz-type inhibitors are particularly appealing because they are able to affect various cellular targets, thereby influencing diverse therapeutic targets.

HMIQ3c1 belongs to a new group of so-called IQ-peptides. This compound displayed neuroprotective properties in mouse neuroblastoma (a form of brain cancer) cells subjected to toxicity induced by beta-amyloid — the major component of senile plaques in Alzheimer’s — and neurotoxin 6-hydroxydopamine (6-OHDA), which causes oxidative stress and impairs cellular production of energy.

HMIQ3c1 increased the viability of cells exposed to beta-amyloid by 39.4%, but did not improve their resistance to 6-OHDA.

According to the scientists, both the newly found peptides in H. magnifica and the previously discovered protease inhibitors in Heteractis crispa — a different species of sea anemone — have considerable pharmacological potential, particularly through their cell-protective and anti-inflammatory properties.

“Chronic inflammation can cause many serious disorders — not only [Alzheimer’s], but also [Parkinson’s], arthritis, pancreatitis, cancer, and other diseases,” Elena Leychenko, one of the study’s authors and a professor at FEFU, said in a press release.

“Proteases are ferments that destroy proteins. They play an important role in the inflammation process and therefore are amidst the most desired targets for new anti-inflammatory medicinal drugs,” Leychenko added.

Although protease inhibitors found in sea anemones have one main function, they may acquire new properties with minor structural changes. Besides neuroprotective compounds, sea anemones also contain molecules with anti-cancer effects. However, a better understanding of their protective properties and how to best combine them requires further work, Leychenko said.

“The manufacture of new generation drugs may be started only after the completion of all trial stages, including pre- and clinical ones. … If the funds are found, the process would still take 3 to 5 years,” she added.

José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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