People with a known, high risk for Alzheimer's disease develop abnormal brain function even before the appearance of telltale amyloid plaques that are characteristic of the disease, according to a new study.

For decades the amyloid hypothesis has dominated the research field in Alzheimer's disease. The theory describes how an increase in secreted beta-amyloid peptides leads to the formation of plaques, toxic clusters of damaged proteins between cells, which eventually result in neurodegeneration. Scientists at Lund University, Sweden, have now presented a study that turns this premise on its head. The research group's data offers an opposite hypothesis, suggesting that it is in fact the neurons' inability to secrete beta-amyloid that is at the heart of pathogenesis in Alzheimer's disease.

Scientists at the UT Health Science Center San Antonio restored learning and memory in an Alzheimer's disease mouse model by increasing a protein called CBP. Salvatore Oddo, Ph.D., of the university's Department of Physiology and Barshop Institute for Longevity and Aging Studies, said this is the first proof that boosting CBP, which triggers the production of other proteins essential to creating memories, can reverse Alzheimer's effects.

A protein associated with Alzheimer's disease clogs several motors of the cell transport machinery critical for normal cell division, leading to defective neurons that may contribute to the memory-robbing disease, University of South Florida researchers report.

UC Santa Barbara scientists have made a discovery that has the potential for use in the early diagnosis and eventual treatment of plaque-related diseases such as Alzheimer's disease and Type 2 diabetes.

Unexpected results from a Scripps Research Institute and ModGene, LLC study could completely alter scientists' ideas about Alzheimer's disease -- pointing to the liver instead of the brain as the source of the "amyloid" that deposits as brain plaques associated with this devastating condition. The findings could offer a relatively simple approach for Alzheimer's prevention and treatment.

In Alzheimer's disease, a protein fragment called beta-amyloid accumulates at abnormally high levels in the brain. Now researchers funded by the National Institutes of Health have found that in the most common, late-onset form of Alzheimer's disease, beta-amyloid is produced in the brain at a normal rate but is not cleared, or removed from the brain, efficiently. In addition to improving the understanding of what pathways are most important in development of Alzheimer's pathology, these findings may one day lead to improved biomarker measures for early diagnosis as well as a new approach to treating this devastating disorder.