Researchers in Tokyo continue encouraging research on oxytocin as a potential Alzheimer’s drug target. When administered nasally, the hormone appeared to reverse cognitive decline in some lab mice.
The hormone oxytocin is involved bonding behaviors. It goes to work during child labor and breastfeeding, but it has also earned its reputation as “the love hormone” for its role in romantic attachment. Now, mounting evidence from a research team in Japan shows it might also play a role in the treatment of neurodegenerative conditions like Alzheimer’s disease.
In 2020, researchers at the Tokyo University of Science conducted a mouse study that suggested that the hormone might be able to reverse some of the harmful effects linked to beta-amyloid, a hallmark protein in Alzheimer’s disease. This month, this team has reinforced these findings in a follow-up study: Their new mouse study, just published in the journal Neuropsychopharmacology Reports, shows that that the hormone actually succeeded at reversing cognitive impairment in lab mice. A cell-penetrating derivative of oxytocin was administered via the rodents’ nasal passages.
In the 2020 study, the team looked at the effects of amyloid-beta peptides in the hippocampus. The new study investigates the effects of this hormone in on, specifically, the spacial memory of mice with cognitive impairment and beta-amyloid build-up in their brains.
Mice that received the nasal dose of the lab’s oxytocin derivative showed memory improvements in one of a few tests: their performance in a certain kind of maze. The big breakthrough here is that the researchers saw that the hormone had successfully dispersed throughout their brains, despite the naturally occurring form of oxytocin’s limited ability to cross the blood brain barrier. Study senior author Jun-Ichiro Oka, Ph.D., professor emeritus at the Tokyo University of Science noted that this is a bid of confidence in the lab’s cell-derived, intranasal administration of the hormone.
“My team is the first to show that the oxytocin derivative can improve [B-amyloid peptide]-induced memory impairment in mice,” Oka said in a news release. “This suggests that oxytocin may help reduce the cognitive decline we see in Alzheimer’s disease.”
Third-party researchers seconded the study’s significance. “This is an important paper in that it demonstrates a putative role for the neuropeptide oxytocin in both protective and somewhat restorative effects against (amyloid-induced) neurodegeneration,” Georgetown University Medical Center professor of neurology and biochemistry James Giordano, Ph.D. told Medical News Today. “Further, it reveals that both endogenous oxytocin [and] exogenously administered oxytocin can exert such effects in an animal model.”
Giordano added that a related neuropeptide, vasopressin, also contributes to memory formation and processing in the mammalian brain.
“This study may shed new light on the interactive roles of neuropeptides in brain health, protection against oxidative stress, and in sustaining neurocognitive functions,” he said. “This research by Akiyoshi Saitoh’s group from the Tokyo University of Science may have implications for research in Alzheimer’s disease, as well as brain drug delivery.”
Animal studies rarely translate into benefits in clinical trials, however; the researchers acknowledge that more study is needed to determine whether these findings could have a positive effect in humans.