How does a memory form? To demonstrate how this process occurs at the most basic level, biophysicists at Tel Aviv University replicated that event with neurons attached to a computer chip. Itay Baruchi and Eshel Ben-Jacob placed neurons from rat embryos on a chip surface and connected 64 electrodes to record activity. The researchers witnessed an identical pattern of nerve firings when chemical stimulants were dropped repeatedly at the same location on the chip. After some time, the neurons began to fire in the same way without chemical activation—the point at which they claim a memory becomes imprinted.
Understanding differences between the proteins made by normal and diseased brain tissues may provide a new approach to diagnostics. Richard D. Smith of the Pacific Northwest National Laboratory and Desmond J. Smith of the University of California, Los Angeles, have created a complex system for analyzing proteins that combines advanced instrumentation with sophisticated image processing to inspect one-millimeter cubes of brain tissue from a pair of normal mice. The investigators determined the abundance of 1,028 proteins in the tissues. Future experiments will use this methodology to compare normal brain tissue with that afflicted by a neurodegenerative disease.
Better diagnostic techniques are needed, in particular, for Alzheimer’s disease. Stina M. Tucker, Esther Oh and Juan C. Troncoso of the Johns Hopkins University School of Medicine demonstrated a test using antibodies that bind to the amyloid-beta proteins that form damaging plaques in the brains of Alzheimer’s patients. The antibodies adhered to proteins in an early stage of a disease that mimics Alzheimer’s in genetically engineered mice. That finding might eventually lead to a test for humans that could be used along with drugs under development to avert the disease through preventive treatment.
Conceivably, that test could be combined with a treatment that uses phages—viruses that infect bacteria—to break up noxious plaque. Beka Solomon of Tel Aviv University showed preliminary proof of this idea by administering phages via a nasal spray to 100 mice genetically engineered to develop Alzheimer’s-like plaques. After a year of treatment, the mice had 80 percent fewer plaques than untreated mice.