Share

Today, we have an interesting study showing that the neuronal damage caused by beta-amyloid, which is associated with Alzheimer’s disease, is repaired when the amyloid is removed [1]. This means that removing amyloid could potentially reverse the symptoms of Alzheimer’s in the early stages of the disease before too much damage is done.

Amyloids are misfolded proteins that stick together to form web-like materials. Probably the best-known form of amyloid is beta-amyloid: the stifling plaques in the brains of patients with Alzheimer’s disease. Misfolded proteins are thought to be one of the primary reasons we age and are described in the landmark aging research paper The Hallmarks of Aging.

These plaques suffocate the neurons and cause them and the brain to slowly die; therefore, finding ways to remove them has been the focus of much research, and finally, after many years, progress is being made. The researchers in this study used a primary neuron model to test this, and the results were impressive. These results support the repair approach that has been advocated by the SENS Research Foundation for over a decade and suggests that clearing amyloids may help restore lost function.

Hopefully, this will move to human clinical trials sooner rather than later, and a number of other drugs are in development to help remove amyloids, some of which are showing potential [2, 3]. Stem cell approaches are also being investigated to clear these amyloids from the brain to restore function [4, 5].

Conclusion

This study is a great proof of concept that Alzheimer’s is not a one-way process and that we can get someone back if we develop the technology to remove amyloids from the body. We could potentially treat age-related diseases like Alzheimer’s more effectively by using repair approaches such as this one, thus keeping ourselves healthier as we grow older.

Literature

[1] Tanokashira, D., Mamada, N., Yamamoto, F., Taniguchi, K., Tamaoka, A., Lakshmana, M. K., & Araki, W. (2017). The neurotoxicity of amyloid β-protein oligomers is reversible in a primary neuron model. Molecular Brain, 10(1), 4.

[2] Krishnan, R., Tsubery, H., Proschitsky, M. Y., Asp, E., Lulu, M., Gilead, S., … & Kirschner, D. A. (2014). A bacteriophage capsid protein provides a general amyloid interaction motif (GAIM) that binds and remodels misfolded protein assemblies. Journal of molecular biology, 426(13), 2500-2519.

[3] Levenson, J. M., Schroeter, S., Carroll, J. C., Cullen, V., Asp, E., Proschitsky, M., … & Shoaga, S. (2016). NPT088 reduces both amyloid-β and tau pathologies in transgenic mice. Alzheimer’s & Dementia: Translational Research & Clinical Interventions, 2(3), 141-155.

[4] Daria, A., Colombo, A., Llovera, G., Hampel, H., Willem, M., Liesz, A., … & Tahirovic, S. (2016). Young microglia restore amyloid plaque clearance of aged microglia. The EMBO Journal, e201694591.

[5] Naaldijk, Y., Jaeger, C., Fabian, C., Leovsky, C., Blüher, A., Rudolph, L., … & Stolzing, A. (2016). Effect of systemic transplantation of bone marrow‐derived mesenchymal stem cells on neuropathology markers in APP/PS1 Alzheimer mice. Neuropathology and applied neurobiology.

CategoryNews, Research
About the author

Steve Hill

Steve serves on the LEAF Board of Directors and is the Editor in Chief, coordinating the daily news articles and social media content of the organization. He is an active journalist in the aging research and biotechnology field and has to date written over 500 articles on the topic as well as attending various medical industry conferences. In 2019 he was listed in the top 100 journalists covering biomedicine and longevity research in the industry report – Top-100 Journalists covering advanced biomedicine and longevity created by the Aging Analytics Agency. His work has been featured in H+ magazine, Psychology Today, Singularity Weblog, Standpoint Magazine, and, Keep me Prime, and New Economy Magazine. Steve has a background in project management and administration which has helped him to build a united team for effective fundraising and content creation, while his additional knowledge of biology and statistical data analysis allows him to carefully assess and coordinate the scientific groups involved in the project. In 2015 he led the Major Mouse Testing Program (MMTP) for the International Longevity Alliance and in 2016 helped the team of the SENS Research Foundation to reach their goal for the OncoSENS campaign for cancer research.
  1. June 21, 2017

    SLEEP: To improve overall health and reduce the risks of developing Alzheimer’s or any disease, focus on the 3 pillars of health: exercise, nutrition, and sleep. Exercise and nutrition are important to provide enough oxygenated blood to brain cells, and one role of sleep is to flush away byproducts of cell metabolism.

    Just as the Lymphatic System helps rid the body of toxins and waste, the Glymphatic System does the same for the brain. Sleep plays a strong role, because as your body sleeps, your brain is acting as mental janitor, clearing out all of the junk that accumulates from daily thinking. During the deepest stages of sleep, neurons actually shrink in size, allowing cerebral fluid to circulate faster to flush out the beta amyloid protein and tau that otherwise can build up as plaque and contribute to Alzheimer’s disease.

    We humans tend to sleep two hours less today than we did before the invention of the electric light bulb, and the amount of sleep we get declines with age. We also produce less of the sleep-inducing hormone Melatonin, which is also the body’s most powerful antioxidant. That’s why my wife and I take supplements at bedtime.
    See “Ability to Remove Alzheimer’s Disease Protein from the Brain Slows with Age” (https://neurosciencenews.com/aging-amyloid-beta-removal-neurology-2389/), including the comments.

Write a comment:

*

Your email address will not be published.

© 2018 - LIFE EXTENSION ADVOCACY FOUNDATION
Privacy Policy / Terms Of Use

       Powered by MMD