Researchers at Boston University have discovered a surprising mechanism in the brains of zebra finches that may explain why humans have a limited ability to regenerate brain cells.

Using high-powered electron microscopy, the team observed neurogenesis — the birth and migration of new neurons. 

The findings challenge previous assumptions about how the brain integrates new cells and repairs itself.

“We found that in songbirds, new neurons in the adult brain behave like explorers forging a path through a dense jungle,” said Benjamin Scott, a BU College of Arts & Sciences assistant professor of psychological and brain sciences and the study’s corresponding author.

Tunneling neurons

While most human organs undergo frequent cellular updates, our brains are largely restricted to the neurons present at birth. 

In contrast, fish, reptiles, and birds experience lifelong neurogenesis, allowing their brains a regular refresh that most mammals lack. 

This disparity has led researchers to investigate why human brain regeneration is so limited and whether the biological mechanisms found in other species can be harnessed to unlock future regenerative therapies for the human brain.

The zebra finch, a small Australian songbird, is a primary subject for neurological research due to its exceptional ability to learn and perfect complex songs. 

Experts gain valuable insights into how animal brains acquire new skills and master intricate sounds by studying vocal learning. 

Boston University discovered that neurogenesis in the zebra finch brain involves a surprisingly aggressive migration process.

In this new work, advanced microscopy was used to observe newborn neurons “tunneling” through the brain — physically shoving and squishing mature cells to reach their destinations — rather than navigating carefully around them. 

This bullying behavior suggests that while the birth of new cells helps the brain repair and learn, it does so through a disruptive mechanism that forces its way into existing neural circuits.

Neurodegenerative diseases

Scott proposes that the disruptive nature of tunneling neurons enables learning and repair; it may also threaten the integrity of existing memories. 

Because our brains are repositories for complex, lifelong memories and intricate personality traits, we simply cannot afford to have bully neurons plowing through our gray matter.

To keep our memories intact, we sacrificed the ability to repair ourselves.

This evolutionary trade-off leaves us more vulnerable to brain disorders and age-related decline. 

However, there’s also an optimistic takeaway: the discovery proves that neurons can migrate without “glia scaffolds” — the biological highways previously thought essential for brain repair.

It suggests that human brain regeneration might be possible even without those lost structures.

“Most glia scaffolds are lost in humans after birth, and this loss was thought to be an obstacle for neurogenesis in the adult brain,” explained Scott. “However, our work shows that new neurons in the bird do not need this glia scaffold. This is exciting because it means that brain repair may not require specialized glia scaffolds.” 

The BU team is now moving to the genetic level. They are using single-cell RNA sequencing to eavesdrop on the “conversations” these tunneling neurons have with their neighbors.

They want to know the “how” and the “why.” How does a neuron know when to stop shoving? And can we teach human cells to do the same?

Scientists hope to unlock fundamental biological secrets that could eventually lead to breakthroughs in human neurology.

The findings were published in the journal Current Biology on April 17.