STEM-Talk

Episode 12: Dale Bredesen discusses the metabolic factors underlying Alzheimer’s Disease


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‘Would you rather remember: the latest episode of Friends, or how to speak?’ asks Dr. Dale Bredesen, a nationally-recognized expert on neurodegenerative diseases.
We don’t have to think about the answer to that question. In fact, we are biologically programmed to preserve speech and forget the television show. But physiological changes occur as we age, which begin to affect our ability to speak, walk, and remember names and faces.
The most extreme and recognizable form of this is Alzheimer’s Disease, which Dr. Bredesen states is the third leading cause of death in the United States. He has come up with a novel therapeutic approach that first investigates the underlying metabolic changes leading to the disease.
Bredesen’s approach, called MEND (metabolic enhancement for neurodegeneration) helped a 65-year-old woman recover her functional memory, after her first physician had written her off as bound to the same demise of her mother, who suffered and died from Alzheimer’s Disease.
Bredesen shares these and other insights in this episode of STEM-Talk, where he and host Dawn Kernagis engage in a rich and thought-provoking conversation about the future of treating neurodegenerative and other diseases.
Bredesen has been on the faculty at UCSF, UCSD. Currently, he divides his time between UCLA and the Buck Institute for Research on Aging, of which he is founder and CEO: http://buckinstitute.org/bredesenLab
For a close-up look at Dr. Bredesen’s work, check out his papers in the Journal Aging: http://www.impactaging.com/papers/v6/n9/full/100690.html ; http://www.impactaging.com/papers/v7/n8/full/100801.html.
As well as is his paper on ApoE4 in the Journal Neuroscience: http://www.ncbi.nlm.nih.gov/pubmed/26791201
00:55: Dawn introduces Dr. Bredesen as a nationally-recognized expert on neurodegenerative diseases such as Alzheimer’s Disease.
1:17: Ford explains that Bredesen’s research has found that AD stems from an imbalance in nerve cell signaling. In the normal brain, specific signals foster memory making, while balancing signals support memory breaking. In AD, the balance of these opposing signals is disturbed. Nerve connections are suppressed, and memories are lost.
1:47: Dawn adds that Bredesen’s findings, which support the view that AD is a metabolically driven, neurodegenerative process, are contrary to the popular belief that the disease is derived from an accumulation of plaques in the brain.
2:50: Ford reads Mark Riff’s 5-star iTunes review: “Fantastic line-up. And what a wealth of cutting edge information. Just having access to these incredible minds is unbelievable. Can’t wait to see what’s coming up.”
3:15: Dawn describes Bredesen’s background: college at Caltech, medical school at Duke University, Chief resident in neurology at UCSF, where he was also a post-doc in Nobel Laureate Stanley Prusiner’s laboratory.
4:02: Bredesen describes how he got into research, first as an undergrad at CalTech. He went to medical school to understand how diseases affect the brain, and specifically alter learning and memory.
4:47: “The whole molecular neuroscience revolution of the 1980s and 1990s has really offered us the novel tools to understand these diseases,” adding that until now, treating and reversing neurodegenerative diseases like Huntington’s and Lou Gehrig’s has been the greatest area of biomedical failure. “This is exciting time where we are starting to develop therapies.”
5:52: The development of large data sets and systems biology is having a major impact on illnesses. People would formerly spend their whole career on one mechanism, but now we’re realizing disease is multi-factorial.
7:05: AD is a network imbalance that is very analogous to osteoporosis. Signals contribute to osteoblastic activity, which is laying down the bones. Other signals contribute to osteoclastic activity, or taking up the bones. For most of our lives, these signals are “beautifully balanced,
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STEM-TalkBy Dawn Kernagis and Ken Ford

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