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.
Scientists at the Gladstone Institutes have deciphered how a protein called Arc regulates the activity of neurons—providing much-needed clues into the brain’s ability to form long-lasting memories.
Lennart Mucke, MD, who directs neurological research at the Gladstone Institutes, today received the MetLife Foundation’s 2013 Award for Medical Research in Alzheimer’s Disease at a scientific briefing and awards ceremony in New York.
Shinya Yamanaka next month will receive the Essey Award for his “Commitment to a Cure” from The ALS Association Golden West Chapter. This annual award represents the exceptional determination, spirit and dedication to the fight against amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease.
Gladstone scientists have discovered that a certain type of DNA damage long thought to be particularly detrimental to brain cells can actually be part of a regular, non-harmful process. The team further found that disruptions to this process occur in mouse models of Alzheimer’s disease—and identified two therapeutic strategies that reduce these disruptions.
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.
Scientists at the Gladstone Institutes have identified a novel mechanism by which a type of low-carb, low-calorie diet—called a “ketogenic diet”—could delay the effects of aging.