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Oxytocin To Prevent or Reverse Alzheimer’s Symptoms?

NEWS RELEASE: Oxytocin as a new therapy to prevent or reverse Alzheimer’s Disease symptoms?

The good news keeps rolling in for oxytocin, everybody’s favorite “love hormone.” As we’ve detailed previously, oxytocin therapy promotes weight loss in humans by decreasing food intake [1], [2], while nevertheless promoting anabolic activity in muscle and bone [3]. New research in an entirely different field is now revealing oxytocin’s remarkable potential in the field of cognitive disorders, specifically Alzheimer’s Disease.

Alzheimer’s Disease can be a long, drawn-out and debilitating illness that slowly robs people of their individuality. Alzheimer’s Disease is the most common cause of dementia in elderly patients, and it is characterized by progressive memory loss and amyloid plaque accumulation in the brain.

Patients suffering from Alzheimer’s Disease develop localized regions of insoluble amyloid proteins (ie. plaques) in brain tissue that prevent healthy blood flow and cellular communication. The link between amyloid plaques in the brain and the development of cognitive deficits has studied extensively [4].

Recent high-impact research from the Tokyo University of Science shows that oxytocin can actually reverse the symptoms of Alzheimer’s Disease in a preclinical setting [5]. Most excitingly, oxytocin can be delivered effectively in a nasal spray format.

Best of all, oxytocin is a natural neuropeptide which is incredibly well tolerated in humans [6], unlike other potential therapeutic options for AD that are still being explored in preclinical research.

oxytocin Proposed mechanism of action

Fig 1. Proposed mechanism of action.  The Alzheimer’s associated amyloid beta plaque protein reduced the levels of NMDA receptors located on the surface of brain cells. Calcium (Ca2+) influx through NMDA receptors is essential for memory formation.  Oxytocin facilitates ERK activation in brain cells. Oxytocin improves brain cell function by activating the MEK/ERK signaling pathway.  Activated ERK triggers more AMPA receptors to be produced.  Oxytocin causes more AMPA receptors to go to the surface of brain cells, and thus allow for normal Ca2+ signaling that is essential for memory formation and retrieval. 

In a press release, senior study author Dr. Akiyoshi Saitoh notes, “This is the first study in the world that has shown that oxytocin can reverse Aβ-induced impairments in the mouse brain.” Of course, this is merely the first step and further research remains to be conducted in alternate preclinical models (and ultimately in humans) before sufficient knowledge can be gathered to repurpose oxytocin into a drug for Alzheimer’s Disease.

Regardless, these results have already ushered in a new direction towards the creation of novel therapies for the treatment of dementia caused by Alzheimer’s Disease.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

References

  1. E. A. Lawson, D. A. Marengi, R. L. Desanti, T. M. Holmes, D. A. Schoenfeld, and C. J. Tolley, “Oxytocin reduces caloric intake in men,” Obesity, 2015.
  2. V. Ott et al., “Oxytocin reduces reward-driven food intake in humans,” Diabetes, 2013.
  3. S. E. McCormack, J. E. Blevins, and E. A. Lawson, “Metabolic effects of oxytocin,” Endocrine Reviews. 2019.
  4. P. T. Nelson, H. Braak, and W. R. Markesbery, “Neuropathology and cognitive impairment in alzheimer disease: A complex but coherent relationship,” Journal of Neuropathology and Experimental Neurology. 2009.
  5. J. Takahashi et al., “Oxytocin reverses Aβ-induced impairment of hippocampal synaptic plasticity in mice,” Biochem. Biophys. Res. Commun., 2020.
  6. J. C. Flanagan, L. M. Sippel, A. Wahlquist, M. M. Moran-Santa Maria, and S. E. Back, “Augmenting Prolonged Exposure therapy for PTSD with intranasal oxytocin: A randomized, placebo-controlled pilot trial,” J. Psychiatr. Res., 2018.

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