Healthy adult brains are endowed with a vast number of synapses, structures that relay signals across nerve cells to enable communications, information processing and storage throughout the nervous system. Apart from dynamic periods when the brain is learning new information or skills, the number of the "glutamatergic" synapses, the major type of synapses that neurons use to activate each other, largely remains constant in adults.
In brain disorders such as Alzheimer's, these synaptic connections, which hold our precious memories, are known to break down too early and disappear. This synapse degeneration is thought to start long before the loss of memory and accelerate as diseases progress. The causes of synapse degeneration in neurodegenerative disorders has not been well understood, mainly because scientists have not yet unraveled the key mechanisms that normally hold together these tiny structures (an average of one micrometer in diameter) throughout our lifetime.
Neurobiologists at the University of California San Diego have now uncovered the long-sought-after mechanisms behind the maintenance of glutamatergic synapses. Based on this fundamental discovery, Division of Biological Sciences Postdoctoral Scholar Bo Feng, Professor Yimin Zou and their colleagues have identified the main components driving amyloid beta-associated synapse degeneration. Amyloid beta are peptides of 36-43 amino acids derived from the amyloid precursor protein (APP) and are the main component of amyloid plaques found in the brains of people with Alzheimer's disease.
