Oxytocin, alternatively referred to as the love or cuddle hormone, is a hormone emitted by the posterior lobe of the pituitary gland, which is located at the base of the brain.
Although it’s exact function remains somewhat ambiguous to us lamens, endocrinologists believe that it plays a substantial role in childbearing, empathy, and social interaction in mammals.
And now, thanks to a new report published in the journal Biochemical and Biophysical Research Communication, we can speculate about one more potential benefit associated with the tend and defend agent.
Pitting mysteries against one another, researchers examine the ways in which oxytocin levels might reduce impairment associated with cognitive decline.
Much of Alzheimer’s destructive pathology is influenced by a toxic buildup of amyloid-beta (Aβ) proteins. Overtime, as the condition progresses, Aβ clumps together to form plaques around neurons in the brain, leading to mental deterioration; more discreetly hindering synaptic plasticity in the hippocampus.
Synaptic plasticity refers to our ability to adapt to varying degrees of neural activity.
Some of the symptoms of this neural disruption include:
- Increased memory loss and confusion.
- Inability to learn new things.
- Difficulty with language and problems with reading, writing, and working with numbers.
- Difficulty organizing thoughts and thinking logically.
- Shortened attention span.
- Problems coping with new situations
In the new report, the authors posit that oxytocin may actually help reverse cognitive damage induced by this buildup.
“Oxytocin, a peptide hormone synthesized in the hypothalamic paraventricular nucleus, has been reported to participate in the regulation of learning and memory performance. However, no report has demonstrated the effect of oxytocin on the amyloid-beta (Aβ)-induced impairment of synaptic plasticity,” the authors wrote in the report. “In this study, we examined the effects of oxytocin on the Aβ-induced impairment of synaptic plasticity in mice.”
“Oxytocin reverses Aβ-induced impairment of hippocampal synaptic plasticity”
The new study employed mice models.
Mice in the experiment group, who evidenced plaque build-ups in their brains, were administered oxytocin. These mice demonstrated improved cognition soon thereafter.
In order to isolate oxytocin as a lone factor, the author blocked the hormone receptors in the subject’s brain, and just as anticipated, the results were not observable.
The mechanisms can only be guessed at this early on but the authors have some theories-most of which revolve around calcium.
Calcium is believed to play a role in facilitating healthy neural signaling as well as the formation of memories. While Ab proteins are believed to mute these relationships in some way.
If either is true, it stands to reason that oxytocin, a hormone believed to support calcium influx in cells, would be an influential deterrent against aggressive modes of dementia.
“This is the first study in the world that has shown that oxytocin can reverse Aβ-induced impairments in the mouse hippocampus,” explained the study’s lead author, Akiyoshi Saitoh in a media release. “At present, there are no sufficiently satisfactory drugs to treat dementia, and new therapies with novel mechanisms of action are desired. “We expect that our findings will open up a new pathway to the creation of new drugs for the treatment of dementia caused by Alzheimer’s disease.”