If our brains rely on thousands of different pathways to function, where do researchers even start for cognitive disease like Alzheimer’s disease (AD)? It’s as complicated as it sounds, but researcher Nikolaos Robakis is able to break the process down for listeners and offer insight on neurodegenerative diseases of the brain.

Listen and learn

• How there are two forms of Alzheimer’s and what molecular biology techniques are used to study them,
• What role risk factors like diabetes and cardiovascular disease play,
• Why they’ve zeroed in on the mutation evident in familial Alzheimer’s and what it might mean for both types, and
• What they hope to understand about the cascade that leads to neurodegeneration.

Nikolaos K. Robakis is a professor of neuroscience and psychiatry at the Icahn School of Medicine at Mt. Sinai. He’s also the A.P. Slaner Professor for Alzheimer’s Disease Research. Fine-tuning the prevention and management of Alzheimer’s disease relies on a clearer understanding of how the neurodegeneration develops, and that’s where Dr. Robakis’ work comes in.

He explains that there are actually two forms of Alzheimer’s disease: one is the genetic form, called familial Alzheimer’s, and the other much more common type that has polymorphic causes is termed the sporadic familial form.

While previously it was thought plaques and tangles in the brain caused Alzheimer’s, researchers like Robakis have found that’s not necessarily true. By creating a model of familial Alzheimer’s, which has a very simple one-gene mutation at its inception, he hopes to learn more about the cascade that leads to the neurodegeneration in both types. While they know about this amino acid mutation, they don’t understand how it leads to neuronal death. He adds, “the central question is, what causes the acceleration in the neuronal death?”

Listen in to find out what they think thus far and how this might contribute to better treatment for dementia patients.

Episode also available on Apple Podcasts: apple.co/30PvU9C

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