When do neurons die




















Some good news, apparently the brain never stops growing! Scientists believe that memory may begin to fail because no new neurons continue to grow in the hippocampus — a part of the brain responsible for memory, emotion and cognition.

Healthy older men and women can generate just as many new brain cells as younger people, it finds. They found that people aged 79 had just as many new neurons forming in the hippocampus as those who were Even the oldest brains produced new brain cells. The groundbreaking findings represent the first time researchers explored newly formed neurons and the state of blood vessels within the entire human hippocampus soon after death.

Such conditions could impact the production of new brain cells. Old and new brains have more in common than we thought Neurogenesis — the ability to generate new hippocampal cells — declines with age in primates. This decreasing production of neurons was believed to occur in ageing humans, too. So, if you keep your brain active, your neurons are more likely to grow. This is true both after injury and in the healthy brain. Some stop signs are part of the sheath, or covering, around neighboring axons, called myelin sheath Figure 1 , left.

Some stop signs are part of a scar that gets built like a protective wall around an injury in an effort to keep the damage from spreading. These scars are made by brain cells called astrocytes star cells, due to their star-like appearance. Scar-building astrocytes are just trying to help, but they also release a chemical into their environment that makes it hard for axons to grow Figure 2. But, there is good news here as well. Scientists are working on strategies to motivate injured neurons to grow by using special growth molecules and to eliminate stop signs for axons in order to make the injury environment more supportive for nerve cell growth [ 1 ].

The immune response plays an essential role in any kind of repair after injury. In injured skin, immune cells will rush to the site of injury from the blood and help the resident immune cells clean up debris from dead cells. Once the clean up is done, the immune cells die and stop the fight. The brain has specialized resident immune cells as well, and they will become activated when they sense danger or damage.

If they continue to spit out toxic chemicals over long periods, they can cause more harm than good, by killing healthy neurons. This is why scientists are trying to understand what switches brain immune cells on and off and trying to figure out how they can modify the response of these immune cells, so the cells can be helpful rather than harmful [ 2 ]. Learning about the limitations of neurons compared to skin cells, you may be disappointed that an organ as important as the brain seems to be unprepared for damaging events.

The truth is, the central nervous system has an ingenious strategy to repair itself that is entirely different from the strategy used by other organs. The brain will never be the same as before the damage, but it will try to compensate for its losses. Neurons in the brain are able to change their connections with each other. This process is called plasticity , and it helps the brain to adapt to the loss of neurons.

Forget for a moment about dying cells, the responsibility for plasticity lies entirely with the surviving cells. How does this work? Apart from growing new arms to connect with new cells, neurons can also modify the strength of existing connections with other neurons Figure 3.

They can either strengthen such connections or they can weaken them, resulting in a totally new network of connections in the brain. This plasticity is driven and directed by activities that we perform. After a stroke or brain injury, patients usually improve to a certain extent doing some sort of physical therapy.

The improvement is not so much due to growth of new neurons, as you learned above, but because these patients keep stimulating plasticity and, therefore, build new connections between surviving neurons in their brains!

Unfortunately, plasticity as a repair mechanism has its limits. Plasticity relies entirely on surviving cells, so the more surviving cells there are, the better. If someone suffers a severe brain injury, or a huge stroke that kills a substantial amount of brain cells, then there are less surviving neurons available for plasticity than following a mild concussion. The more cells available for plasticity to work with, the more plasticity can occur.

This is why severe central nervous system injuries usually result in lasting disabilities. These cause signals to be sent to neurons nearby. If one neuron receives enough signals from the excitatory neurons around it, then that neuron may be excited enough to exhibit its own action potential. Action potentials are the codes that our brain uses to perform computations that support our perception, cognition, and action control. If a neuron stops exhibiting action potentials long enough, it will starve.

To reduce age-related brain shrinkage, Professor Vishton recommends that you keep your brain active. Physical activity—even moderate exercise like walking—inspires neural activation and even the creation of new neurons in certain areas of the brain such as the hippocampus.

One of the best ways to inspire broad-based neural activity, however, is to try new things. As we become more experienced at some activity—playing a particular sport, for example—our brain becomes faster and more accurate in producing the proper actions at the right moments in time. On the contrary, we learn to use less and less of our brain, developing specialized circuits that rapidly, automatically mediate the task performance. Peter M. By Peter M.

Professor Vishton explains the mechanisms behind this process and how you can replace dead neurons. With aging, just as the body requires continued exercise to remain functional and strong, so does the brain.

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