Super Brain (4 page)

By then, other evidence was confirming that peripheral nerves like the vagus can heal when cut. (You can experience the same phenomenon if a deep gash leaves your finger numb; after a time feeling returns.) But for centuries people had believed that nerves in the central nervous system (the brain and spinal cord) lacked the same ability.

It’s true that the central nervous system cannot regenerate with the same robustness and rapidity of the peripheral nervous system.

DIAGRAM 1: NEURONS AND SYNAPSES

Nerve cells (neurons) are true wonders of nature in their ability to create our sense of reality. Neurons connect to each other to form vast and intricate neural networks. Your brain contains over 100 billion neurons and up to a quadrillion connections, called
synapses
.

Neurons project wormlike threads known as axons and dendrites, which deliver both chemical and electrical signals across the gap between synapses. A neuron contains many dendrites to receive information from other nerve cells. But it has only one axon, which can extend out to over a meter (roughly 39 inches) in length. An adult human brain contains well over 100,000 miles of axons and countless dendrites—enough to wrap around the Earth over four times.

However, due to “neuroplasticity,” the brain can remodel and remap its connections following injury. This remapping is the functional definition of neuroplasticity, which is now a hot-button issue.
Neuro
comes from
neuron
, while
plasticity
refers to being malleable. The old theory was that infants mapped their neural networks as a natural part of their development, after which the process stopped and the brain became hardwired. We now view the projections of nerve cells in the brain like long thin worms continually reconfiguring themselves in response to experience, learning, and injury. To heal and to evolve are intimately linked.

Your brain is remodeling itself right now. It doesn’t take an injury to trigger the process—being alive is enough. You can promote neuroplasticity, moreover, by exposing yourself to new experiences. Even better is to deliberately set out to learn new skills. If you show passion and enthusiasm, all the better. The simple step of giving an older person a pet to take care of instills more willingness to live. The fact that the brain is being affected makes a difference, but we need to remember that neurons are servants. The dissecting knife reveals changes at the level of nerve projections and genes. What really invigorates an older person, though, is acquiring a new purpose and something new to love.

Neuroplasticity is better than mind over matter. It’s mind turning into matter as your thoughts create new neural growth. In the early days, the phenomenon was scoffed at and neuroscientists were belittled for using the term
neuroplasticity
. Still, many new concepts that will likely be seminal and mainstream decades from now are today judged meaningless and useless. Neuroplasticity overcame a rough start to become a star.

That mind has such power over matter was momentous for both of us in the 1980s. Deepak was focused on the spiritual side of the mind-body connection, promoting meditation and alternative medicine. He was inspired by a saying he ran across early on: “If you want to know what your thoughts were like in the past, look at your body
today. If you want to know what your body will be like in the future, look at your thoughts today.”

For Rudy, this paradigm-breaking discovery really hit home when he was a graduate student at Harvard Medical School in the neuroscience program. Working at Boston Children’s Hospital, he was trying to isolate the gene that produces the main brain toxin in Alzheimer’s disease, the amyloid beta protein—the A beta peptide for short—the sticky substance that accumulates in the brain and correlates with neurons becoming dysfunctional and breaking down. Rudy was furiously poring over every paper he could find on Alzheimer’s and this toxic amyloid. It can take the form of the beta-amyloid in Alzheimer’s disease, or the prion amyloid in Mad Cow–related diseases.

One day he read a paper showing how the brain of an Alzheimer’s patient had dealt with the accumulation of beta-amyloid in an effort to remodel the stricken part of the brain responsible for short-term memory, the hippocampus, which is located in the temporal lobe (so called because it is located in the skull beneath the temples).

The fact that the brain could try to find a way to bypass devastating damage changed Rudy’s entire view of the disease he had been studying day and night in a snug lab the size of a small supply room on the fourth floor of the hospital. Between 1985 and 1988, he focused on identifying the gene that makes beta-amyloid accumulate excessively in the brains of Alzheimer’s patients. Every day he worked side by side with his colleague Rachel Neve, while in the background a music soundtrack played, especially by Keith Jarrett, arguably the best jazz pianist who has ever lived.

Rudy loved Keith Jarrett’s concerts for their brilliant improvisation. Jarrett had his own word for it: “extemporized.” In other words, they were on the spot, radically spontaneous. To Rudy, Jarrett expressed in music the way the brain works in the everyday world—responding in the moment in creative directions based on the foundation of a lifetime’s worth of experiences. Wisdom
renewing itself in the moment. Memory finding fresh life. It is fair to say that when Rudy discovered the first Alzheimer’s gene, the amyloid precursor protein (APP) in that small fourth-floor lab, his muse was Keith Jarrett.

Against this background enters the paper in 1986 that gave hope for Alzheimer’s patients to regenerate brain tissue. It was an unseasonably cold day even for a Boston winter, and Rudy was sitting in the open stacks on the third floor of the library at Harvard Medical School, breathing the familiar scent of old musty paper—some of these scientific papers hadn’t seen the light of day for decades.

Among the new articles on Alzheimer’s was one in the journal
Science
, reported by Jim Geddes and colleagues, with the intriguing title “Plasticity of Hippocampal Circuitry in Alzheimer’s Disease.” After glancing through it, Rudy sprinted to the change machine to get a handful of dimes for the copy machine. (The luxury of computerized journals was still in the future.) After carefully reading it together with Rachel, they stared at each other wide-eyed for what seemed hours, finally exclaiming, “How cool is that!?” The mystery of a brain that could heal itself had entered their lives.

The essence of that seminal study was this. In Alzheimer’s disease, one of the first things that goes wrong is short-term memory. In the brain, the key neural projections that allow sensory information to be stored are literally severed. (We are in the same field as Cruikshank when he cut a dog’s vagus nerve.) More specifically, there is a small swollen bag of nerve cells in the brain called the entorhinal cortex, which acts as a way station for all the sensory information you take in, relaying it on to the hippocampus for short-term storage. (If you can remember that Rudy was working with a colleague named Rachel, that’s the hippocampus doing its job.) The hippocampus takes its name from the Latin word for seahorse, which it resembles. Make two C’s out of your thumb and forefinger on each hand facing each other and then interlock them in a parallel plane, and that is roughly the right shape.

Let’s say you come home from shopping and want to tell a friend about some red shoes that would be perfect for her. The image of those shoes, passing through the entorhinal cortex, is relayed via neural projections called the perforant pathway. Now we have arrived at the physiological reason why someone with Alzheimer’s will not remember those shoes. In Alzheimer’s patients the exact region where the perforant pathway pierces the hippocampus routinely contains an abundance of neurotoxic beta-amyloid, which short-circuits the transfer of sensory information. Adding to the damage, nerve endings begin to shrink and break down in the same region, effectively severing the perforant pathway.

The nerve cells in the entorhinal cortex that should be sprouting those nerve endings soon die because they rely on growth factors, the proteins that support their survival, to be shunted up the nerve endings that once connected to the hippocampus. Eventually, the person can no longer achieve short-term memory and learning, and dementia sets in. The result is devastating. As one saying goes, you don’t know you have Alzheimer’s because you forget where you put your car keys. You know you have Alzheimer’s when you forget what they are for.

In his seminal study, Geddes and his colleagues showed that in this area of massive neuronal demise, something nothing short of the magical occurs. The surviving neighboring neurons begin to sprout new projections to compensate for the ones that were lost. This is a form of neuroplasticity called compensatory regeneration. For the first time, Rudy was encountering one of the most miraculous properties of the brain. It was as if a rose were plucked from a bush, and the bush next to it handed it a new rose.

Rudy suddenly had a deep appreciation for the exquisite power and resilience of the human brain. Never count the brain out, he thought. With neuroplasticity, the brain has evolved into a marvelously adaptable and remarkably regenerative organ. Hope existed that even in a brain being damaged by Alzheimer’s, one need only
catch it early enough, and neuroplasticity may be triggered. It’s one of the brightest possibilities for future research.

Myth 2. The brain’s hardwiring cannot be changed

During all the time before neuroplasticity was proved to be legitimate, medicine could have listened to the Swiss philosopher Jean-Jacques Rousseau, who argued in the middle 1700s that nature was not stagnant or machinelike but alive and dynamic. He went on to propose that the brain was continually reorganized according to our experiences. Therefore, people should practice mental exercise the same as physical exercise. For all intents and purposes, this may have been the first declaration that our brains are flexible and plastic, capable of adapting to changes in our environment.

Much later, in the middle of the twentieth century, American psychologist Karl Lashley provided evidence for this phenomenon. Lashley trained rats to seek out food rewards in a maze and then removed large portions of their cerebral cortex, bit by bit, to test when they would forget what they had previously learned. He assumed, given how delicate brain tissue is and how totally dependent a creature is on its brain, that removing a small portion would lead to severe memory loss.

Shockingly, Lashley found that he could take out 90 percent of a rat’s cortex, and the animal still successfully navigated the maze. As it turned out, in learning the maze, the rats create many different types of redundant synapses based on all their senses. Many different parts of their brains interact to form a variety of overlapping sensory associations. In other words, the rats were not just seeing their way to the food in the maze; they were smelling and feeling their way as well. When bits of the cerebral cortex were removed, the brain would sprout new projections (axons) and form new synapses to take advantage of other senses, using the cues that remained, however tiny.

Here we have the first strong clue that “hardwiring” should be greeted with skepticism. The brain has circuitry but no wires; the
circuits are made of living tissue. More important, they are reshaped by thoughts, memories, desires, and experiences. Deepak remembers a controversial medical article from 1980 entitled, half in jest, “Is the Brain Really Necessary?” It was based on the work of British neurologist John Lorber, who had been working with victims of a brain disorder known as hydrocephalus (“water on the brain”), in which excessive fluid builds up. The pressure that results squeezes the life out of brain cells. Hydrocephalus leads to retardation as well as other severe damage and even death.

Lorber had previously written about two infants born with no cerebral cortex. Yet despite this rare and fatal defect, they seemed to be developing normally, with no external signs of damage. One child survived for three months, the other for a year. If this were not remarkable enough, a colleague at Sheffield University sent Lorber a young man who had an enlarged head. He had graduated from college with a first-class honors degree in mathematics and had an IQ of 126. He had no symptoms of hydrocephalus; the young man was leading a normal life. Yet a CAT scan revealed, in Lorber’s words, that he had “virtually no brain.” The skull was lined with a thin layer of brain cells about a millimeter thick (less than one-tenth of an inch), while the rest of the space in the skull was filled with cerebral fluid.

This is an appalling disorder to contemplate, but Lorber pushed on, recording more than six hundred cases. He divided his subjects into four categories depending on how much fluid was in the brain. The most severe category, which accounted for only 10 percent of the sample, consisted of people whose brain cavity was 95 percent filled with fluid. Of these, half were severely retarded; the other half, however, had IQs over 100.

Not surprisingly, skeptics went on the attack. Some doubters said that Lorber must not have read the CAT scans correctly, but he assured them that his evidence was solid. Others argued that he hadn’t actually weighed the brain matter that remained, to which he drily replied, “I can’t say whether the mathematics student has a brain
weighing 50 grams or 150 grams, but it is clear that it is nowhere near the normal 1.5 kilograms.” In other words, 2 to 6 ounces may be involved, but that’s nowhere near 3 pounds. More sympathetic neurologists declared that these results were proof positive of how redundant the brain is—many functions are copied and overlap. But others shrugged off this explanation, noting that “redundancy is a cop-out to get around something you don’t understand.” To this day, the whole phenomenon is shrouded in mystery, but we need to keep it in mind as our discussion unfolds. Could this be a radical example of the mind’s power to have the brain—even a drastically reduced brain—carry out commands?