Northwestern studies SuperAgers to better understand what is going right in their brains. Credit: Northwestern
Key Points:
- SuperAger neurons are even larger than those in individuals 20 to 30 years younger.
- These neurons do not have tau tangles that are a hallmark of Alzheimer’s.
- Larger neurons in the brain’s memory region are a biological signature of SuperAging trajectory.
The Northwestern SuperAging Research Program studies unique individuals known as SuperAgers, 80+ year-olds who show exceptional memory at least as good as individuals 20 to 30 years their junior.
In a new study, researchers show that these SuperAgers actually carry a unique biological signature that comprises larger and healthier neurons in the entorhinal cortex that are relatively void of tau tangles.
“To understand how and why people may be resistant to developing Alzheimer’s disease, it is important to closely investigate the postmortem brains of SuperAgers,” said lead author Tamar Gefen, an assistant professor of psychiatry and behavioral sciences at Northwestern University. “What makes SuperAgers’ brains unique? How can we harness their biologic traits to help elderly stave off Alzheimer’s disease?”
For the study, scientists examined the brains of six SuperAgers, seven cognitively average elderly individuals, six young individuals and five individuals with early stages of Alzheimer’s.
The results indicate that SuperAgers harbor large, healthier neurons in layer II (of VI) of the entorhinal cortex compared with their same-aged peers, individuals with early stages of Alzheimer’s disease and even individuals 20 to 30 years younger. The researchers also showed that these large layer II neurons were spared from the formation of tau tangles.
Taken together, the findings suggest that a neuron spared from tangle formation can maintain its structural integrity (i.e., remain healthy and large). The inverse also seems to be true: Tau tangles can lead to neuronal shrinkage.
“In this study, we show that in Alzheimer’s, neuronal shrinkage in the entorhinal cortex appears to be a characteristic marker of the disease,” said Gefen. “We suspect this process is a function of tau tangle formation in the affected cells leading to poor memory abilities in older age. Identifying this contributing factor (and every contributing factor) is crucial to the early identification of Alzheimer’s, monitoring its course and guiding treatment.”
Future studies are needed to understand how and why neuronal integrity is preserved in SuperAgers. Specifically, Gefen said she wants to focus on probing the cellular environment. She also plans to investigate other hubs along the memory circuit of the brain to better understand the spread of or resistance to disease.
Information provided by Northwestern University.