spring newsletter

In This Issue:

  • Clinical Genetics Research at UCLA Easton Center ADRC
  • Dementia Brain Bank at the Easton Center
  • New Additions to the Easton Center
  • Clinical Trials
  • Upcoming Events

The Mary S. Easton Center for Alzheimer’s Disease Research at UCLA has very active teams working on basic research, drug discovery, biomarkers for early diagnosis and clinical activity including clinical trials, cognitive testing, and patient care.

Clinical Genetics Research at UCLA Easton Center ADRC

Ariadna Martinez, M.S., C.G.C.

By: Ariadna Martinez, MS, CGC, Genetic Counselor

Through efforts taking place around the country and the world, including at the Mary S. Easton Center for Alzheimer’s Research and Care at UCLA (Easton Center), scientists have begun to identify the various factors that contribute to the development of Alzheimer’s disease (AD) and related conditions. These discoveries have enabled us to identify individuals at increased risk for AD, allowing for early diagnosis, and have paved the way for research aimed at identifying and developing preventive measures and treatments that one day could be tailored to each individual.

The term Alzheimer’s disease includes different presentations of the condition that differ in terms of age of onset of symptoms and the presence of a family history of this condition. In the early form of Alzheimer’s disease, also known as Early-Onset Alzheimer’s Disease (EOAD), individuals tend to show symptoms in their ‘30s to ‘60s. Some of these patients have relatives in each generation with the condition and have a form of AD called familial AD. In the late 1980s, with the help of families that participated in research studies, scientists learned that the presence of a damaging genetic change (mutation) in one of three genes, amyloid precursor protein (APP), Presenilin 1 (PSEN1) and Presenilin 2 (PSEN2), was the cause of familial AD in the participating families. Research is currently taking place to identify potential genetic causes of other cases of familial AD and to develop potential treatments to restore the normal functions of the proteins made by these genes.

Continue reading the article