Antidepressant May Slow Progression of Alzheimer’s Disease

According to research by the Washington University School of Medicine, published in Science Translational Medicine, a common antidepressant can reduce the production of brain plaques.

 

Brain plaques correlate closely with memory problems and other cognitive impairments caused by Alzheimer’s disease. Stopping plaque buildup is believed to help halt the mental decline of Alzheimer’s patients. Scientists found the antidepressant citalopram stopped the growth of plaques in a mouse model of the disease. The research also found, in young adult humans who were cognitively healthy, that a single dose of the antidepressant lowered production of amyloid beta by thirty-seven percent. The researchers stress that while the results may be promising, any treatment at this point is premature.

 

Levels of amyloid beta, a protein produced by normal brain activity, rise in the brains of patients with Alzheimer’s, and eventually clump together to form plaques. Most antidepressants keep serotonin circulating in the brain, and this study was born from the theory that serotonin helps reduce plaque levels in cognitively health individuals.

 

For this research, scientists gave citalopram to older mice with brain plaques. They used two-photon imaging to track the growth of plaques in the mice for twenty-eight days. The results showed a rate of formation of new plaques decreased by seventy-eight percent. In a second experiment, the scientists gave citalopram to twenty-three people cognitively healthy people aged eighteen to fifty. Spinal fluid from the participants over the next day showed a thirty-seven percent drop in amyloid beta production.

 

Sources:

  1. Sheline YI, West T, Yarasheski K, Swarm R, Jasielec MS, Fisher JR, Ficker WD, Yan P, Xiong C, Frederiksen C, Grzelak MV, Chott R, Bateman RJ, Morris JC, Mintun MA, Lee J-M, Cirrito JR. An antidepressant decreases CSF Ab production in healthy individuals and in transgenic AD mice. Science Translational Medicine, online May 14, 2014.
  2. Washington University in St. Louis. (2014, May 14). Antidepressant may slow Alzheimer’s disease. ScienceDaily. Retrieved May 16, 2014 from sciencedaily.com/releases/2014/05/140514142326.htm

By Emma Henson

The Roskamp Institute is a 501(c)3 research facility dedicated to translating the efforts of its qualified research staff into real-world results for those suffering from neurological diseases. To learn more about our programs and to get information about donating, visit www.rfdn.org.

Advertisements

Amino Acids Improve Sleep in Mice with Traumatic Brain Injury

A study by Oregon Health and Science University, published in Science Translational Medicine, discovered a way to fix sleep disturbances in mice with traumatic brain injury. These results are important, because people commonly experience long-term and severe sleep and wakefulness issues after suffering concussions, a mild form of traumatic brain injury. The research hinged on feeding mice branched chain amino acids, something humans naturally produce from food. Dr. Miranda Lim, first author of the study, hopes that further studies will uphold the results found, and a dietary supplement prescribed as a viable therapy for concussions could be developed.

 

Nearly two million people in the US suffer traumatic brain injury every year, and nearly 72% have sleep disturbances. Sleep problems are not only frustrating, but physically harmful. The lack of rest impairs attention and memory formation for TBI patients, who already have a higher rate of functional disability and higher cost of rehabilitation. Treatments to remedy the dangerous swelling occurring after TBI exist, while underlying brain damage evident in sleep impairment as well as learning patterns remains without treatments.

 

The study compared mice with mild TBI to uninjured mice, and found the injured mice much less capable of staying awake for sustained periods of time. Scientists pinned this on underactive orexin neurons, meant to maintain wakefulness, mirroring spinal fluid evidence of human TBI patients. The scientists gave the injured mice a dietary therapy of branched chain amino acids; the building blocks of neurotransmitters, chemicals released by neurons in the brain. The results showed a restoration of normal orexin levels, and improved wakefulness. This offers a proof-of-principle for dietary intervention as a treatment for TBI, and hopefully an avenue to help brain-injured patients regain cognitive functions.

 

Source:

  • M. Lim, J. Elkind, G. Xiong, R. Galante, J. Zhu, L. Zhang, J. Lian, J. Rodin, N. N. Kuzma, A. I. Pack, A. S. Cohen. Dietary Therapy Mitigates Persistent Wake Deficits Caused by Mild Traumatic Brain Injury. Science Translational Medicine, 2013; 5 (215): 215ra173 DOI: 10.1126/scitranslmed.3007092
  • Oregon Health & Science University (2013, December 11). Dietary amino acids improve sleep problems in mice with traumatic brain injury. ScienceDaily. Retrieved January 7, 2014, from http://www.sciencedaily.com­ /releases/2013/12/131211185331.htm

By Emma Henson

The Roskamp Institute is a 501(c)3 research facility dedicated to translating the efforts of its qualified research staff into real-world results for those suffering from neurological diseases. To learn more about our programs and to get information about donating, visit www.rfdn.org.