Novel Look At Brains of Diabetics

A $2 million grant to UC Davis researchers will fund one of the first studies investigating how diabetes may contribute to memory loss and possibly Alzheimer's disease in older people, aided by advanced imaging techniques that show the functioning brain.

Charles DeCarli, professor of neurology and director of the UC Davis Alzheimer's Disease Center, and his colleagues recently were awarded the grant from the Larry L. Hillblom Foundation to study the impact of diabetes on aging and memory loss. The grant will fund a four-year study that will focus on the brains of diabetics, looking at how the disease changes the brain and whether information is processed any differently in a diabetic's brain compared to those without the disease.

Medical advancements have improved life expectancy and contribute who are 65-and-older being the fastest-growing segment of the population. Many in this age group, particularly those older than 75, experience memory loss. Additionally, age is the single-greatest risk factor for Alzheimer's disease, with a doubling of the risk every five years after 65. An increasing number of senior citizens also suffer from chronic illnesses, such as hypertension, heart disease and diabetes.

Scientists do not know how diabetes, which impairs the body's ability to control the amount of sugar in the blood, might be contributing to Alzheimer's disease, a progressive neurological disorder caused by changes in brain tissue with age. Both diabetes and Alzheimer's are associated with memory loss that can lead to dementia. Studying how memory works in diabetics is a crucial first step in unraveling the puzzling interaction between these two diseases.

The team will do this using the latest brain imaging techniques. For example, to determine which parts of the diabetic's brain are involved in memory, researchers will take images of a patient's brain using functional magnetic resonance imaging (fMRI) while the participant is performing a memory task. These images will tell them which parts of the brain are active during these tasks.

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Potential Alzheimer's Disease Drug Target Identified

In findings with the potential to provide a therapy for Alzheimer's disease patients where none now exist, a researcher at the University of California, San Diego and colleagues have demonstrated in mice a way to reduce the overproduction of a peptide associated with the disease. The study, which showed substantial improvement in memory in an animal model of Alzheimer's disease, was led by Vivian Y. H. Hook, Ph.D., professor of the Skaggs School of Pharmacy and Pharmaceutical Sciences and professor of neurosciences, pharmacology and medicine at the UCSD School of Medicine, together with American Life Science Pharmaceuticals of San Diego. The study will be published in the March 21 edition of the Journal of Biological Chemistry, online March 14.

A hallmark sign of Alzheimer's disease, seen during autopsy of a patient's brain, is the accumulation of amyloid plaque deposits composed primarily of the neurotoxic beta-amyloid (Aβ) peptide which is believed to be a major factor in the cause of the disease. The Aβ peptides are "cut" out from a larger protein called the amyloid precursor protein (APP) and bind together to form plaques in brain regions responsible for memory. One drug strategy to fight Alzheimer's disease is to reduce production of Aβ."We discovered two chemical compounds that inhibit a new enzyme target, leading to reduced production of beta amyloid and improved memory in a mouse model of Alzheimer's disease," said Hook.

Cancer-Related Protein vs Alzheimer's disease

The cancer-related protein Akt may profoundly influence the fate of the tau protein, which forms bundles of tangled nerve cell fibers in the brain associated with Alzheimer's disease, reports a new study led by researchers at the University of South Florida and the Mayo Clinic in Jacksonville, FL.

The study was published online in the early edition of the Proceedings of the National Academy of Sciences. The findings may provide another piece of the puzzle in figuring out how tau proteins can poison nerve cells in the brain.

Akt is known to increase cancer cell survival capability and has become a target in the development of some cancer-inhibitor drugs. The abnormal accumulation of tau protein tangles kills nerve cells and is considered one of the hallmarks of Alzheimer's disease. "This study describes for the first time a new function for the cancer-related protein Akt - one that may help promote Alzheimer's disease pathology," said lead author Chad Dickey, PhD, assistant professor of molecular pharmacology and physiology at USF. "We found that increased amounts of Akt may prevent the removal of abnormal proteins, such as tau, causing these proteins to accumulate and disrupt the balance within the cells."

While this Akt-induced imbalance might result in cancer cells continuing to divide uncontrollably, Dr. Dickey suggests it likely has a different effect in Alzheimer's disease. "The nerve cells may try to divide in the brain, but cannot, and therefore die," he said. "Thus regulating levels of Akt, rather than its activity, may be beneficial to sufferers of diseases of aging, such as cancer, Alzheimer's and even diabetes."

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