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 . 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].
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.
 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.
 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.
 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.
 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.
 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.