A new Northwestern Medicine study found that memory-related neurons in the entorhinal cortex were much bigger in SuperAgers than in cognitively average peers, people with early-stage Alzheimer’s disease, and even people 20 to 30 years younger than SuperAgers who are 80 years and older.
Tau tangles, which are a sign of Alzheimer’s disease, were not found in these neurons.
“The remarkable observation that SuperAgers showed,” remarks lead author Tamar Gefen, “larger neurons than their younger peers may imply that large cells were present from birth and are maintained structurally throughout their lives.”
The authors “conclude that larger neurons are a biological signature of the SuperAging trajectory.”
The study of SuperAgers with great memories was the first to show that these people have a unique biological signature that includes larger, healthier neurons in the entorhinal cortex (pathology) that are mostly free of tau tangles.
The findings of this study were published in The Journal of Neuroscience today.
The Northwestern SuperAging Research Program studies people who are called “SuperAgers.” These are people who are 80 years old or older and have great memories, at least as good as people 20 to 30 years younger than them.
“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,” Gefen added. “What makes SuperAgers’ brains unique? How can we harness their biologic traits to help elderly stave off Alzheimer’s disease?”
Scientists looked at the brain’s entorhinal cortex as it governs memory and is one of the first places that Alzheimer’s disease attacks. Six layers of neurons tightly stacked on top of one another make up the entorhinal cortex. In particular, Layer II acts as a relay station for information traveling between different parts of the brain’s memory circuit.
In the research, scientists show that the neurons in layer II of the entorhinal cortex of SuperAgers are bigger and healthier than those in the same age group, in the early stages of Alzheimer’s disease, and in people 20 to 30 years younger than them. They also demonstrated that the development of tau tangles spared these substantial layer II neurons.
Together, the results indicate that a neuron that is spared from tangle development can continue to function normally (i.e., remain healthy and large). Tau tangles can result in neuronal atrophy, which appears to be true in reverse.
The SuperAger project participants offer their brains to science.
Six SuperAgers, seven seniors with average cognitive function, six children, and five people with early-stage Alzheimer’s disease were used in the study. The size of neurons in layer II of the entorhinal cortex was then assessed (compared to layers III and V). They also assessed if tau tangles were present in these patients.
For reasons that are still not clear, certain groups of cells in the entorhinal cortex are more likely to form tau tangles during normal aging and the early stages of Alzheimer’s disease.
“In this study, we show that in Alzheimer’s, neuronal shrinkage (atrophy) in the entorhinal cortex appears to be a characteristic marker of the disease,” Gefen added.
“We suspect this process is a function of tau tangle formation in the affected cells leading to poor memory abilities in older age,” Gefen said. “Identifying this contributing factor (and every contributing factor) is crucial to the early identification of Alzheimer’s, monitoring its course and guiding treatment.”
Future research is required to determine how and why SuperAgers maintain neuronal integrity. Gefen wants to concentrate on examining the cellular setting.
“What are the chemical, metabolic or genetic features of these cells that render them resilient?” she asked.
She also wants to look into other hubs along the brain’s memory circuit to learn more about how diseases spread or how people fight them off.
Image Credit: Getty
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