The early stages of Alzheimer's disease are thought to occur at the synapse, since synapse loss is associated with memory dysfunction. Evidence suggests that amyloid beta (Aß) plays an important role in early synaptic failure, but little has been understood about Aß's effect on the plasticity of dendritic spines.
These spines are short outgrowths of dendrites (extensions of neurons) that relay electrical impulses in the brain. A single neuron's dendrite contains hundreds of thousands of spines, providing memory storage and transmission of signals across the synapse -- the junction where such nerve impulses occur. Plasticity of these spines, or the ability to change and grow, is essential for the transmission of signaling in the brain.
Researchers led by Roberto Malinow, MD, PhD, professor of neurosciences and Shiley-Marcos Endowed Professor in Alzheimer's Disease Research at the University of California, San Diego School of Medicine, have shed more light on how Aß's destructive effects on the brain are related to its impact on the plasticity of dendritic spines. Their study was published on December 27 in the journal Nature Neuroscience.