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Protein Changes Identified In Early-Onset Alzheimer’s

January 10, 2012

Discovery may lead to better understanding of the disease, possible therapies

With a lack of effective treatments for Alzheimer’s, most of us would think long and hard about whether we wanted to know years in advance if we were genetically predisposed to develop the disease. For researchers, however, such knowledge is a window into Alzheimer’s disease’s evolution.

Understanding the biological changes that occur during the clinically “silent” stage – the years before symptoms appear – provides clues about the causes of the disease and may offer potential targets for drugs that will stop it from progressing.

In a new study, researchers at UCLA have identified chemical changes taking place in the brains of people destined to develop familial Alzheimer’s disease at least 10 years before symptoms or diagnoses occur. Reporting in the current online edition of the journal Archives of Neurology, John Ringman, a UCLA associate professor of neurology, and colleagues identified changes in 56 proteins, including increases in the amyloid protein long associated with Alzheimer’s, inflammatory markers and other proteins related to the brain’s synapses, the connections between neurons through which these brain cells communicate with each other.

Familial Alzheimer’s and sporadic, late-onset Alzheimer’s are distinct forms of what many consider a single disease. The majority of Alzheimer’s cases are sporadic and late-onset, developing after age 65; the causes of this disease type are not completely understood but are at least partly genetic. Familial Alzheimer’s (FAD), a rare form of the disease caused by certain gene mutations, affects less than 2 percent of patients. It is typically early-onset, developing before age 65, and it is inherited – all offspring in the same generation have a 50




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