I don’t usually write about early or animal-phase research, but this is potentially quite important for those dealing with dementia, related illnesses, and brain injury.
The protein amyloid beta is believed to be the major cause of Alzheimer’s disease. This protein basically clogs cells and causes neurotransmitters in cells to become hyperactive, generating noise that interferes with thinking and memory.
That leaves three interesting questions:
- What triggers the production of this protein?
- Is there a way to shut production of the protein down?
- What happens if we do?
A team of researchers at the University of Munich (Germany) have identified one such substance, of a category known as BACE inhibitors, that is effective in reducing the amount of amyloid beta in brain cells. Tested in mice, with the inhibitor included in their food for eight weeks, the result when beyond what the researchers expected:
As expected, the mice had less amyloid beta in their brain after this period, since its production was inhibited. However, the effect of the substance was much more far-reaching: the animals’ brain functions actually normalized. There were fewer hyperactive nerve cells, and the slow-wave brain patterns once again resembled those in healthy mice. A key finding for the scientists was the observation that the animals’ memory also improved.
(1 is the original journal article; 2 is the report in Science Daily for non-technical readers.)
Basically, functioning was restored to a level comparable to healthy animals who had never had the disease.
These researchers are planning a human clinical trial.
What makes this a really big deal is that amyloid beta is also a factor in traumatic brain injury (TBI). This presents a possible and quick route to restoration of brain function for both dementia and TBI victims. It is not a “cure” for either, but for the victim and their family, the potential is life-changing.
It’s amazing what you can find buried in a list of breaking scientific news.
- A. D. Keskin, M. Kekuš, H. Adelsberger, U. Neumann, D. R. Shimshek, B. Song, B. Zott, T. Peng, H. Förstl, M. Staufenbiel, I. Nelken, B. Sakmann, A. Konnerth, and M. A. Busche. BACE inhibition-dependent repair of Alzheimer’s pathophysiology. Proceedings of the National Academy of Sciences, 2017 DOI: 10.1073/pnas.1708106114
- Technical University of Munich (TUM). “Dementia: BACE inhibitor improves brain function: BACE inhibitor successfully tested in Alzheimer’s animal model.” ScienceDaily. ScienceDaily, 28 July 2017. <www.sciencedaily.com/releases/2017/07/170728100937.htm>
- Hong YT, Veenith T, Dewar D, Outtrim JG, Mani V, Williams C, Pimlott S, Hutchinson PJ, Tavares A, Canales R, Mathis CA, Klunk WE, Aigbirhio FI, Coles JP, Baron JC, Pickard JD, Fryer TD, Stewart W, Menon DK. Amyloid imaging with carbon 11-labeled Pittsburgh compound B for traumatic brain injury. JAMA Neurol. 2014 Jan;71(1):23-31. PubMed.
- ALZFORUM, “Imaging Reveals Amyloid Up To a Year After Traumatic Brain Injury,” 16 November 2013. http://www.alzforum.org/news/research-news/imaging-reveals-amyloid-year-after-traumatic-brain-injury
- VE Johnson et. al., “Traumatic brain injury and amyloid-β pathology: a link to Alzheimer’s disease?” Nat Rev Neurosci. 2010 May;11(5):361-70. doi: 10.1038/nrn2808.
- Rebekah C. Mannix and Michael J. Whalen, “Traumatic Brain Injury, Microglia, and Beta Amyloid,” International Journal of Alzheimer’s Disease, Volume 2012 (2012), Article ID 608732, 5 pages. http://dx.doi.org/10.1155/2012/608732