Alzheimer Disease

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The causes of Alzheimer disease and attempts to predict who is at risk for it have been confounding the medical profession ever since Dr Alzheimer first described the disorder in 1906. Finally, a breakthrough in dye and imaging technology may be the key to solving the puzzle.

A discovery about the brain protein KIBRA, commonly found in the kidneys and brain, could lead to future treatments for Alzheimer disease (AD). Investigators at the Translational Genomics Research Institute (TGen), lead by Corneveaux and Liang, in Phoenix found that the risk for AD is 25% lower in persons who carry the memory-enhancing KIBRA gene.1 This fi nding indicates that there might be a link between KIBRA and some of the proteins with which it interacts.

Increased plasma cortisol levels (correlated with increased hypothalamic-pituitary-adrenal axis activity) may be associated with more rapid disease progression in Alzheimer-type dementia (AD). In a study conducted at the Washington University School of Medicine in St Louis, Dr John Csernansky and colleagues assessed 33 patients with very mild or mild AD and 21 persons without AD annually for up to 4 years, using the Clinical Dementia Rating Scale and various neuropsychological tests. Plasma was obtained from each patient and assessed for cortisol level.

The second report from the Alzheimer's Disease Cholesterol-Lowering Treatment (ADCLT) trial was recently published, along with several reviews of clinical and laboratory investigations of the statins, in a theme issue of Acta Neurologica Scandinavica. The accumulated data reflect the potential of the agents to affect the onset or course of Alzheimer disease (AD), with contradictory or insufficient evidence of treatment effect.