Alzheimer’s disease (AD) is a devastating neurodegenerative illness characterized by memory loss, cognitive decline and widespread destruction of neurons in the brain. More than 5 million Americans have symptoms of AD but even more frightening is the escalating number of people who will develop this condition in the future—unless a cure is uncovered. Robert Nagele, PhD, and his team at SOM have opened a huge window into the mystery of this modern scourge.

To make this startling finding, begin with the knowledge that a principal component of the amyloid plaques that devastate the Alzheimer brain is amyloid ß, a 42 amino acid peptide fragment or Aß42. Nagele’s team understood that, despite extensive literature on these proteins, their precise origin, mode of formation and specific contribution to AD remained controversial. “Amyloid beta peptides are abundant in the blood but are unable to cross the blood brain barrier in healthy individuals,” he explains. “Our research now shows that these peptides can readily penetrate through defects in the barrier that result from degenerative conditions common to vascular systems of older individuals.” Atherosclerosis, strokes, hemorrhages, tumors, traumatic brain injury or other conditions can compromise the integrity of the blood/brain barrier. “We found that once these peptides leak into brain tissue, they selectively bind to neurons in the brain that are most affected by Alzheimer’s”—cells that are critical to memory and higher thinking. Theoretically, healthy individuals, even those with neuron-binding autoantibodies in their blood, could hold the development of AD at bay by maintaining good cardiovascular health through diet and exercise. Nagele says, “Our hope is also that these results will spark development of new therapeutics aimed at lowering blood levels of Aß42 or reinforcing the integrity of the blood/brain barrier, which could slow progression or better yet, circumvent this devastating illness altogether.”