The so-called “love hormone” oxytocin may normally be associated with memory impairment but new research indicates it might stave off at least some of the amnesic effects of Alzheimer’s disease.
The hormone oxytocin is known to have varying effects in people, in which it either strengthens or weakens a person’s memory, depending on their personality and genetic makeup.
Post-mortem examinations of people with Alzheimer’s disease found increased levels of oxytocin in memory-related areas of their brain, showing at least some link between the love hormone, memory and one of the most grim neurodegenerative diseases humans face.
People with Alzheimer’s experience a buildup of a toxic form of a peptide called beta-amyloid, the non-toxic form of which is believed to regulate, protect and repair the central nervous system.
The peptide’s toxic form, however, can form plaques on the brain which can, in turn, kill neurons and cause memory loss. Even short-lived exposure to this toxic form can trigger the brain’s own immune system and can cause it to harm neurons rather than protecting them.
This entire immune response can disrupt synaptic plasticity, the mechanism responsible for our ability to both learn and remember.
In a new study, researchers explored this nexus of memory, love hormone and neurodegenerative disease by treating male mice brains with toxic beta-amyloid to confirm the peptide’s negative effects on the aforementioned synaptic plasticity.
They then treated additional brain samples from the same set with a combination of toxic beta-amyloid and oxytocin, and found that the negative impacts of the beta-amyloid were stopped by the oxytocin.
However, when treated with just oxytocin, the researchers observed no effect on synaptic plasticity.
In other words, oxytocin itself cannot prevent or reverse cognitive issues associated with Alzheimer’s on its own, as there is a multitude of factors that lead to overall cognitive decline in a variety of different ways that extend beyond the formation of plaques from accumulation of toxic beta-amyloid.
It does, however, show early promise for mitigating some of the nastiest effects of Alzheimer’s disease, should the research findings be replicable in future clinical trials.
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