This could lead to pharmaceutical therapies and preventive measures to offset these mutations and stop the advancement of early-onset familial Alzheimer's disease. We hope that the information gained from this finding can eventually be applicable to understanding the causes of all forms of Alzheimer's disease. In virtually all cases, according to the UCI researchers, people born with mutant presenilin genes will develop the early form of this neural disease. According to the National Institute on Aging, an estimated 4 million people in the United States suffer from Alzheimer's disease, an incurable form of dementia that primarily strikes the elderly and causes severe memory loss. It is estimated that several hundred thousand of these Alzheimer's cases are due to mutations in the presenilin genes.
Researchers believe that the majority of the cases involve multiple factors.
While genetic predisposition has been well established, other potential risk factors cited include stress, prior head injury and an abnormal concentration of metals in the brain, including zinc, copper and lead. The UCI researchers hope that future research will establish exactly how calsenilin produces its effects. Based on their other research with presenilin, the researchers speculate that calsenilin might regulate the total amount of calcium that is stored inside cells. Tritia R. Yamasaki assisted Leissring, LaFerla and Parker with this research. The study was supported by the National Institutes of Health, a National Research Service Award and a Glenn Scholarship from the American Federation for Aging Research.