Alzheimer’s: Why the Hippocampus is Hit First
- A new collaborative research project at the Fralin Biomedical Research Institute at Virginia Tech aims to understand how mitochondrial dysfunction contributes to the early stages of alzheimer's disease,...
- Researchers are focusing on the entorhinal cortex-hippocampus circuit, a brain region critical for memory and one of the first areas affected by Alzheimer's disease.
- "this new collaborative project brings together my work on synapses and Shannon's on mitochondria in a way that addresses a big gap in the Alzheimer's disease field," Farris...
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Virginia researchers Investigate Mitochondrial Role in early alzheimer’s Advancement
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A new collaborative research project at the Fralin Biomedical Research Institute at Virginia Tech aims to understand how mitochondrial dysfunction contributes to the early stages of alzheimer’s disease, possibly opening new avenues for diagnosis and treatment.
Uncovering the Link Between Mitochondria and Synapses
Researchers are focusing on the entorhinal cortex-hippocampus circuit, a brain region critical for memory and one of the first areas affected by Alzheimer’s disease. The project, led by Assistant Professor Valérie Farris and Professor Shannon Swanger, combines Farris’s expertise in synapses with Swanger’s work on mitochondria.
“this new collaborative project brings together my work on synapses and Shannon’s on mitochondria in a way that addresses a big gap in the Alzheimer’s disease field,” Farris stated in a Virginia Tech News article.
Mitochondrial Overload and Calcium Signaling
Mitochondria, often called the “powerhouses of the cell,” are essential for providing energy for neuronal functions, including synaptic transmission. In Alzheimer’s disease,these structures become impaired.Farris and Swanger hypothesize that mitochondria in the vulnerable memory circuit become overloaded with calcium, a crucial signaling molecule. This overload could contribute to the early breakdown of memory circuits.
“The connection between these cells is one of the first to fail in Alzheimer’s,” Farris explained. “We found that this synapse has unusually strong calcium signals in nearby mitochondria — so strong we can see them clearly under a light microscope. Those kinds of signals are hard to ignore. It gives us a model where we can really watch what’s happening as things start to go wrong.”
Calcium signaling is a complex process vital for synaptic plasticity – the brain’s ability to strengthen or weaken connections between neurons. Disruptions in calcium homeostasis are increasingly recognized as a key factor in neurodegenerative diseases like alzheimer’s. Research published in the journal Neurochemistry International details the intricate relationship between calcium dysregulation and mitochondrial dysfunction in Alzheimer’s.
Research Methodology and State Support
The researchers will compare brain tissue from healthy mice and mice exhibiting Alzheimer’s-like pathology. By analyzing mitochondrial function and synaptic dialogue in both groups, they aim to identify early indicators of stress or failure within the entorhinal cortex-hippocampus circuit. this comparative approach will help pinpoint specific changes occurring at the cellular level before significant cognitive decline is observed.
The project is supported by state-level funding,which Farris emphasized is crucial for enabling Virginia-based researchers to tackle significant health challenges. “This kind of state-level support is critical,” Farris said. “It gives researchers in Virginia the chance to ask questions that may eventually make a difference for peopel living with Alzheimer’s.It’s meaningful to be part of research that could help people facing that journey.”
Farris and Swanger
