Irvine, Calif., December 2, 2024 — In a new study recently published in Scientific Reports, researchers at the UC Irvine Charlie Dunlop School of Biological Sciences have identified a novel way to potentially protect nerve cells in neurodegenerative diseases, opening new possibilities for future treatments. Led by Assistant Professor Katherine Thompson-Peer, the research team discovered that a minor injury to dendrites — structures in neurons responsible for receiving signals — can activate protective regrowth mechanisms in degenerating nerve cells. This finding offers fresh hope for conditions like Huntington’s disease and spinocerebellar ataxias, where progressive cell loss leads to severe cognitive and physical decline.
Neurodegenerative diseases frequently present with early signs of dendrite loss, a damaging structural breakdown that impedes a neuron’s ability to process information. “Loss of dendrites, which are specialized structures that nerve cells use as antennae to gather signals from the environment or from other nerve cells, is one of the early cellular changes observed in neurodegenerative diseases,” said Professor Thompson-Peer. “In this paper, we provide evidence that activating dendrite regeneration pathways has the potential to slow — or even sometimes reverse — dendrite loss. Our findings suggest that a slight injury can activate beneficial regrowth processes in the cell, similar to pruning a tree to encourage new growth.” Interestingly, this regenerative response appears specific to dendrite injury, highlighting a unique pathway for possible treatment across various neurodegenerative conditions.
Using Drosophila (fruit fly) models, the team tested how dendrite injury affected neurons experiencing degeneration due to genetic mutations resembling those in human neurodegenerative diseases. The results were promising, as first author Sydney Prange, and graduate student in the Thompson-Peer lab, explains: “We are able to show not only that neurodegeneration does not prevent regeneration but also that activating regeneration can be neuroprotective in neurodegenerative disease models.” This process of neuroprotection could delay or mitigate neuron loss, possibly alleviating cognitive and physical symptoms often associated with these diseases.
The study’s findings don’t just promise new treatments — they also set a foundation for future research. Prange emphasizes the need to further understand the mechanisms behind this effect, noting, “A key area for future research will be studies to determine the underlying mechanism that supports the neuroprotection we observe. If we can determine what pathways are responsible for the neuroprotection, we can identify new therapeutic targets for neurodegenerative disease-modifying therapies.”
This breakthrough reveals the nervous system’s own resilience, suggesting it may be harnessed to counteract degeneration. The research team encourages ongoing exploration and support to fully unlock the therapeutic potential of this discovery, hoping to pave the way for treatments that preserve health and cognitive function in those facing neurodegenerative disease.
About the University of California, Irvine Charlie Dunlop School of Biological Sciences:
Recognized for its pioneering research and academic excellence, the Charlie Dunlop School of Biological Sciences plays a crucial role in the university’s status among the nation’s top 10 public universities, as ranked by U.S. News & World Report. It offers a broad spectrum of degree programs in the biological sciences, fostering innovation and preparing students for leadership in research, education, medicine and industry. Nestled in a globally acclaimed and economically vibrant community, the school contributes to the university’s impact as Orange County’s largest employer and a significant economic contributor. Through its commitment to exploring life’s complexities, the Dunlop School embodies the UCI legacy of innovation and societal impact. For more on the Charlie Dunlop School of Biological Sciences, visit https://www.bio.uci.edu/.