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as 40 years old, and is passed down directly from generation to generation. The root cause of Alzheimer's has yet to be discovered due to the complexity of how the disease develops in the brain. According to Ringman, patients typically go from what we consider normal to severely impaired in four to 12 years. For patients and their families, being able to distinguish between memory loss common with aging and Alzheimer's disease is important. "Normal changes of cognition in aging differentiating them from early Alzheimer's can be tricky," says Ringman. "A gross example I use is, I don't get worried about people who lose their car keys, I get worried about people who lose their car." Understanding Plaques and Tangles: Although researchers are still not sure what causes Alzheimer's, proteins such as plaques and tangles are viewed as the catalysts in cell death and tissue loss in the brain. Before symptoms are present to patients and their families, these distinct pathological changes seem to materialize. The scientific consensus is that beta-amy- loid peptide - a sticky glue-like protein deposit in the brain- is the first signs of Alzheimer's development. These plaques are abnormal clusters that build up between nerve cells. Amyloid plaques can develop 10 to 15 years be- fore any symptoms of the disease appear, and seem to be the key to prevention development. "We have great new tools for studying the earliest molecular changes of Alzheimer's disease," says Senior Author and Director of USC Alzheimer's Therapeutic Research Institute at Keck School of Medicine Paul Aisen. As the leading figure in Alzheimer's research for more than two decades, Aisen helped develop the earliest Alzheimer's medications patients still use today. "This gives us a highly promising strategy for developing effective treatment," he says. "We do have treatments today and they do help, but they don't change the course of the disease. They only offer modest relief of symptoms. We can do much better than that and we think that the most promising strategy is to focus on this amyloid peptide." Tau protein, the other facet to decoding the Alzheimer's mystery, forms into neuro- fibrillary tangles in the brain shortly after amyloid growth accumulates. These tangles cultivate in brains areas important for memory then spread over time. Scientists believe tau development represents the beginning stage of symptomatic Alzheimer's. Although it's imperative to note that a positive amyloid PET scan does not signify that one will absolutely get Alzheimer's. "You wouldn't want to diagnose someone based on an amyloid scan…Many people will grow old and die with a positive amyloid pet scan and not have Alzheimer's disease," says Professor of Psychiatry and Neurology at Keck School of Medicine and Director of California's Alzheimer's Disease Center Lon Schneider. Schneider is in the process of conducting an eight-year prevention study to develop an amyloid vaccine in adult's who have a substan- tial risk of developing the disease from their genetic disposition. "We're taking people who don't have symptoms at all. They don't necessarily have a positive amyloid pet scan but do carry the APOE-4 gene, which gives them a higher risk of developing Alzheimer's disease," says Schneider. "We're using an anti-amyloid vac- cine, essentially. Injecting particles of synthetic amyloid to cause antibodies against amyloids. We hope that the series of vaccines—essential- ly booster shots—will create enough antibodies that it will endogenously remove amyloid on its own when it's forming." This study comes with its own set of chal- lenges. The recruitment pool, those who pos- sess two copies of the APOE-4 gene represent only 3 percent of the population. According to Schneider, it could take up to 12 years to recruit participants, conduct the study, and then if all goes as planned, get FDA approval and sent out on the market. With Great Power Comes Great Responsibility: Numerous prevention and treatment trials for the disease are actively recruiting adults with focus on reducing Alzheimer's symptoms and slowing or stopping the disease. Individuals with or without dementia are encouraged to partici- pate. By doing so, the public can provide valuable insight into potential treatments for Alzheimer's patients today and for future generations. "Without the generous participation of volunteers in our studies, we cannot develop effective treatment. If more people join our effort in participating in clinical research it would accelerate our work," says Aisen. These technological breakthroughs in medicine being achieved at Keck Medicine of USC have given researchers the gift of crucial discoveries that they needed for helping current and future Alzheimer's patients struggling with a debilitating disease. This brings a renewed sense of hope for finding methods for preven- tion, or even a possible cure down the road. "While we've been working on this disease for a long time and don't yet have highly effective approved drugs, we're getting very close," says Aisen. "We're very excited about studies that are underway or are just getting started. We think that with the coming years, we are going to bring substantial advancement so there is a very hope- ful, upbeat view in the field right now." "We have great new tools for studying the earliest molecular changes of Alzheimer's disease," says Senior Author and Director of USC Alzheimer's Therapeutic Research Institute at Keck School of Medicine Paul Aisen. As the leading figure in Alzheimer's research for more than two decades, Aisen helped develop the earliest Alzheimer's medications patients still use today. 58 SEPTEMBER 2017