In comparison with other primates, our brains are exceptionally large. Why?
A brand new study comparing neurons from different primates pinpointed several genetic changes unique to humans that buffer our brains’ ability to handle on a regular basis wear and tear. Dubbed “evolved neuroprotection,” the findings paint an image of how our large brains gained their size, wiring patterns, and computational efficiency.
It’s not nearly looking into the past. The outcomes could also encourage recent ideas to tackle schizophrenia, Parkinson’s disease, and addiction brought on by the gradual erosion of 1 sort of brain cell. Understanding these wirings may spur artificial brains that learn like ours.
The results haven’t yet been reviewed by other scientists. But to Andre Sousa on the University of Wisconsin-Madison, who wasn’t involved within the work, the findings might help us understand “human brain evolution and all the possibly negative and positive things that include it.”
Larger Brain, Larger Price
Six million years ago, we split from a standard ancestor with our closest evolutionary relative, the chimpanzee.
Our brains rapidly exploded in size—but crucially, only in certain regions. Certainly one of these was on the front of the brain. Called the prefrontal cortex, it’s an “executive control” center that lets us reason, make difficult decisions, and exercise self-control. One other region, buried deep within the brain, processes emotions and offers us the power to simply move with only a thought.
The 2 regions are in ready communication, and their chatter may give rise to parts of our intellect and social interactions, comparable to theory of mind—where we are able to gauge one other person’s emotions, beliefs, and intentions. Dopamine neurons, a sort of brain cell, bridge this connection.
They could sound familiar. Dopamine, which these neurons pump out, is often called the “feel-good” molecule. But they achieve this way more. Dopamine neurons are spread across the complete brain and infrequently dial the activity of certain neural networks up or down, including those regulating emotion and movement. Dopamine neurons are like light dimmers—relatively than brain networks flipping on or off like an easy switch, the neurons fine-tune the extent of motion.
These cells “coordinate multiple points” of brain function, wrote study writer Alex Pollen on the University of California, San Francisco and colleagues.
The puzzle? In comparison with our primate relatives, we only have twice the variety of dopamine neurons, a measly increase in comparison with the expansion of brain size. By scanning the brains of humans and macaque monkeys—which are sometimes utilized in neuroscience research—the team found that our prefrontal cortex is eighteen times larger, and the striatum has ballooned roughly 7 times.
In other words, each dopamine neuron must work harder to produce these larger brain regions.
Though they’ve long “branches,” neurons aren’t passive wires. To attach and performance normally, they require high amounts of energy. Most of this comes from the cells’ energy factories, pea-like structures called mitochondria. While highly efficient, neurons degrade as we age or in cases of neurodegeneration, including Parkinson’s disease.
Dopamine neurons are also especially vulnerable to decay in comparison with other kinds of neurons because making dopamine generates toxic byproducts. Called reactive oxygen species, these chemicals are like tiny bullets that destroy the cells’ mitochondria and their outer wrappers.
Dopamine neurons have several natural methods of fighting back. They pump out antioxidants and have evolved ways to buffer toxic molecules. But eventually these defenses break down—especially in an even bigger brain. In turn, the connection between the “reasoning” and “emotion” parts of the brain starts to fray.
Accumulating damage to those neural workhorses needs to be a nonstarter for constructing larger, more complex brains during evolution. Yet in some way our brains mostly skirted the trauma. The brand new study asked how.
Evolution in a Dish
The team grew 3D blobs manufactured from stem cells from human, chimpanzee, orangutan, and macaque monkeys. After a month, the hybrid mini-brains began pumping out dopamine.
It might sound like a wierd strategy, but pooling cells from different species establishes a baseline for further genetic evaluation. Because they’re all growing in the identical environment in a single blob, any differences in a cell’s gene expression are likely resulting from the species it got here from, relatively than environmental conditions or other effects, explained the team.
The ultimate pool included cells from eight humans, seven chimpanzees, one orangutan, and three macaque monkeys.
The cells worked well together, developing an overall pattern mimicking dopamine neurons across the striatum—ones that reach out to the frontal parts of the brain. After growing them for as much as 100 days, the team captured genes from each cell to gauge which of them were turned on or off. In total, they analyzed over 105,000 cells.
In comparison with other species, human stem cells seemed most versatile. They gave birth not only to dopamine neurons, but in addition other brain cell types. They usually had one other edge: In comparison with chimpanzees, human dopamine neurons dialed up genes to tackle damaging reactive oxygen “bullets.”
Gene expression tests showed that human dopamine cells had far higher levels of several genes that break down the toxic chemicals in comparison with other non-human primates—in turn limiting their damage to the sensitive neurons.
When challenged with a pesticide that elevates reactive oxygen species, human brain cells fought off the assault with a lift of a nurturing protein called brain-derived neurotrophic factor (BDNF). The molecule has long been a neuroscience darling for its ability to spur the birth and growth of recent neurons and rewire old ones. Scientists have suggested BDNF may help ketamine reverse depressive symptoms by reshaping the brain’s networks.
In contrast, chimpanzee neurons from the identical mini-brains couldn’t boost the protective protein when doused with the pesticide.
Carry on Fighting
The team analyzed the hybrid mini-brains at a really early stage of their development, when there was no probability of them developing any kind of sentience.
Their goal was to know how our brains—especially dopamine neurons—have grow to be resilient against damage and might tolerate the energy costs that include a bigger brain.
But the outcomes could also boost cellular defense systems in individuals with dopamine-related disorders. Mutations in protective genes present in the study, for instance, may increase disease vulnerability in some people. Testing them in animal models paves the way in which for more targeted therapies against these disorders.
Knowing how dopamine works within the brain at a molecular level across species provides a snapshot of what sets us other than our evolutionary cousins. This “can advance our understanding of the origins of human-enriched disorders and discover recent therapeutic targets and techniques for drug development,” wrote the team.
