In brain disorders such asAlzheimer’s, is known the degeneration of the synapses, which contain our memories, break too soon and disappear. This synapse degeneration is thought to begin long before memory loss and accelerate as disease progresses.
Localization of signaling components of the Wnt / PCP pathway in glutamatergic synapses in the adult hippocampus detected by super-resolution microscopy. B. Schematic diagram showing the balance of Wnt / PCP signaling in synapse maintenance and the binding site of oligomeric amyloid beta. Credit: Feng et al., Sci. Avv. 2021
The causes of this form of degeneration in neurodegenerative disorders have not been well understood, mainly because scientists have not yet unraveled the key mechanisms that normally hold these tiny structures (an average of one micrometer in diameter) together throughout life.
Healthy adult brains, on the other hand, have a large number of synapses, structures that transmit signals through nerve cells to enable communication, processing and storage of information throughout the nervous system. Aside from the dynamic periods when the brain is learning new information or skills, the number of “glutamatergic” synapses, the main type of synapse neurons use to activate each other, remains largely constant in adults.
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THE search results have been published in the scientific journal Science Advances.
Synapse degeneration: key mechanisms discovered
Neurobiologists ofUniversity of California to San Diego have discovered the long-sought mechanisms underlying the maintenance of glutamatergic synapses. Based on this fundamental discovery, Bo Feng, postdoctoral fellow of the Division of Biological Sciences, Professor Yimin Zou and their colleagues identified the main components that drive synapse degeneration associated withbeta amyloid. Beta amyloids are 36-43 amino acid peptides derived from the amyloid precursor protein (APP) and are the main component of the amyloid plaques found in the brains of people with Alzheimer’s disease.