Joint Gladstone-UCSF study reveals long-life gene also improves learning, memory; opens new path for treating Alzheimer's, age-related diseases
Scientists at the Gladstone Institutes have discovered how the interplay between two proteins in the brain fuels the degradation and death of the class of brain cells, or neurons, that leads to Parkinson’s. These findings, which stand in stark contrast to conventional wisdom, lay much-needed groundwork for developing treatments that target the disease’s elusive underlying mechanisms.
Alzheimer’s disease is one of the greatest challenges facing modern medicine, but there is new hope in the fight against this deadly disease. Today, renowned Alzheimer’s researcher and founding president of the Gladstone Institutes, Robert Mahley, MD, PhD, has received a Seeding Drug Discovery Award from the Wellcome Trust.
For some, the disease multiple sclerosis (MS) attacks its victims slowly and progressively over a period of many years. For others, it strikes without warning in fits and starts. But all patients share one thing in common: the disease had long been present in their nervous systems, under the radar of even the most sophisticated detection methods. But now, scientists at the Gladstone Institutes have devised a new molecular sensor that can detect MS at its earliest stages—even before the onset of physical signs.
There is no easy way to study diseases of the brain. Extracting brain cells, or neurons, from a living patient is difficult and risky, while examining a patient’s brain post-mortem usually only reveals the disease’s final stages. And animal models, while incredibly informative, have frequently fallen short during the crucial drug-development stage of research. But scientists at the Gladstone Institutes and the University of California, San Francisco (UCSF) have taken a potentially more powerful approach: an advanced stem-cell technique that creates a human model of degenerative disease in a dish.
Neurodegenerative diseases are often associated with the buildup of toxic proteins that lead to neuronal death. But now, scientists at the Gladstone Institutes have discovered that the progression of disease is not due to the buildup of toxins itself, but rather in the individual neurons’ ability to dissolve them. Further, they have identified a therapeutic target that could boost this ability, thereby protecting the brain from the diseases’ deadly effects.
The power of the brain lies in its trillions of intercellular connections, called synapses, which together form complex neural “networks.” While neuroscientists have long sought to map these complex connections to see how they influence specific brain functions, traditional techniques have yet to provide the desired resolution. Now, by using an innovative brain-tracing technique, scientists at the Gladstone Institutes and the Salk Institute have found a way to untangle these networks. Their findings offer new insight into how specific brain regions connect to each other, while also revealing clues as to what may happen, neuron by neuron, when these connections are disrupted.
Inside each of us is our own internal timing device, but the inner-workings of this so-called “circadian clock” are complex, and the molecular processes behind it have long eluded scientists. But now, researchers at the Gladstone Institutes have discovered how one important protein falls under direct instructions from the body’s circadian clock. Furthermore, they uncover how this protein regulates fundamental circadian processes—and how disrupting its normal function can throw this critical system out of sync.