AD is progressive, eventually impacting the abilities to recognize close family members, regulate mood and judgment, motor function, understand language, and engage in activities of daily living.
The most significant risk factors for the disease, in addition to biological aging, are family history and genetics. There is no cure for Alzheimer’s.*
Progress in AD Research
Scientists are studying every aspect of the disease to better understand how intrinsic biological aging, genetics, environment, and lifestyle factors influence its development and progression. Such research has the potential to lead to rational modes of prevention, early diagnosis, and effective treatment. MetLife Award winners are continuing to make significant contributions towards those goals.
Here are only a few selected examples, many of which have led to MetLife Awards:
In January 2011, the FDA endorsed a new brain scan that can detect the plaques that indicate AD in a living brain. If approved, the technology, which built on the work of William E. Klunk, MD, PhD, and Chester A. Mathis, PhD, will make it possible to definitively diagnose AD in living patients for the first time. Pioneering investigations on imaging of the living brain have also been carried out by last year’s Award winners, Marcus E. Raichle, MD, and Randy L. Buckner, PhD.
Research projects across the globe, including those led by John Hardy, PhD, Peter St. George Hyslop, MD, Gerard D. Schellenberg, PhD, and Rudolph E. Tanzi, PhD, have discovered rare mutations in three different genes causing dominant forms of AD. In 1993, Allen D. Roses, MD, discovered that those who carry one copy, or even worse, two copies of a relatively common variant of the APOE gene (APOE4) have greatly increased risks of developing AD. In 2011, large groups of investigators led by Gerard D. Schellenberg and colleagues, uncovered common variants in five additional genes that increased the risk of AD. That research required unprecedentedly large and independent samples of genetic data from AD patients.
- Amyloid Plaques
Ongoing insights into the location and composition of the plaques and tangles that devastate brain function in AD will enable investigators to develop treatments that will intervene in the underlying processes of the disease, not just the symptoms. The plaques contain aggregates of smaller derivatives of a large protein called the beta amyloid precursor protein. Edward H. Koo, MD, and Todd Golde, MD, PhD, among others, have made important contributions to our understanding how processing of that protein leads to dangerous forms of amyloid. More recently, Rudolph E. Tanzi and colleagues at Massachusetts General Hospital made surprising observations that these plaques may be the result of attempts by the brain’s innate immune system to fight invading microorganisms.
- Neurofibrillary tangles
While not specific for AD, these tangles result from modifications of a different protein called tau. Basic research on the nature of this pathology has been carried out by many groups, including a husband and wife team in Hamburg, Germany – Eckhard Mandelkow, PhD, and Eva-Maria Mandelkow, PhD.
Each of these findings—like all the research supported by MetLife Foundation Awards for Medical Research—brings us closer to a cure.
For more information:
Contact the National Institute on Aging for more information about these studies and additional resources about Alzheimer's disease at 1-800-438-4380 or visit www.nia.nih.gov/Alzheimers.
*Information about Alzheimer's disease courtesy of the Alzheimer's Association.