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You know how your cells die all the time and new ones are made to replace them, so you practically have a new body every maybe 5 years?
Many people say you become a completely different person every several years, but what about neural cells, do they get replaced?
I believe it would cause a lot of information to get lost if this happened.
By brain cells, I'll assume you mean neurons (the other type are called glial cells). Yes, new neurons arise in a least certain parts of the brain, and yes, they do cause memories to weaken or disappear. This has been shown in mice, guinea pigs and degus.
It would be wrong to assume that neurogenesis occurs with the frequency of, say, gastric cell or skin turnover. Up until recently, it was not thought to occur at all.
Learning and remembering use various cortical structures, including the hippocampus.Throughout life, new neurons (neurogenesis) are continuously added to the dentate gyrus. These additions remodel hippocampal circuits, and when this occurs after memory formation, this neurogenesis leads to degradation or forgetting of established memories. This was shown in adult mice. Conversely, decreasing neurogenesis after memory formation decreased forgetting.
It is not only plasticity that makes the brain adaptable to continuous changes in environmental demands. Adult-born neurons integrate into preexisting neuronal networks and participate in information processing. Adult neurogenesis itself is a type of circuit plasticity required for hippocampus-dependent learning and memory recall. Adult hippocampal neurogenesis may also promote forgetting.
The more neurogenesis there is, the more memories are broken down. Since we retain many memories over our lifetime, it's pretty safe to say out brains don't "turn over" every five years (or even over longer periods); some parts of our brain don't seem to undergo neurogenesis at all.
 Hippocampal Neurogenesis Regulates Forgetting During Adulthood and Infancy Science 9 May 2014
 A Price to Pay for Adult Neurogenesis Science 9 May 2014
 Neurogenesis in the Adult Brain The Journal of Neuroscience February 1, 2002
Addition to anongoodnurse's answer.
Different organisms have different numbers of neurogenic niches (regions where neurons form). For example zebrafish has six niches compared to two in mammals and it is known to have active neurogenesis throughout life. In mammals, apart from the dentate gyrus (subgranular zone) of hippocampus, the other prominent neurogenic niche is the subventricular zone (SVZ) - the region adjoining the ventricles. Immature neurons born at the SVZ migrate to olfactory bulb via the rostral migratory stream[2, 3].
You can also refer to this detailed review  on Adult Neurogenesis.
 Lindsey, Benjamin W., Audrey Darabie, and Vincent Tropepe. "The cellular composition of neurogenic periventricular zones in the adult zebrafish forebrain." Journal of Comparative Neurology 520.10 (2012): 2275-2316.
 Pencea, Viorica, et al. "Neurogenesis in the subventricular zone and rostral migratory stream of the neonatal and adult primate forebrain." Experimental neurology 172.1 (2001): 1-16.
 Bath KG, Lee FS. "Neurotrophic Factor Control of Adult SVZ Neurogenesis". Developmental neurobiology. 2010;70(5):339-349
 Ming, Guo-li, and Hongjun Song. "Adult neurogenesis in the mammalian brain: significant answers and significant questions." Neuron 70.4 (2011): 687-702.
Get Smart: Brain Cells Do Regrow, Study Confirms
March 6, 2000 (Boston) -- Here's hope for those who fear they lost too many brain cells to youthful dissipation: Researchers at Cornell University have demonstrated that cells from an area of the brain essential for learning and memory can regenerate in a laboratory dish. In the future, the discovery might lead to strategies for replacing brain cells lost to diseases such as Alzheimer's.
Until recently, conventional medical wisdom held that we are born with all the brain cells, or neurons, that we'll ever have and when they're gone, they're gone for good. Over the last few years, though, researchers have shown that in at least one area of the brain, a region known as the hippocampus, there is continual turnover of cells throughout most of our lives.
In the latest study, Steven A. Goldman, MD, from Cornell University Medical College in New York City, and colleagues took samples of tissues from the hippocampus that had been removed from patients undergoing surgery to repair brain disorders. They were able to tease out cells from a certain area where populations of "seed," or precursor, cells are found. The researchers were able to separate these precursor cells from mature cells, which can no longer divide. They were able to aid the cells in continuing to divide and grow.
Jack P. Antel, MD, and colleagues from McGill University in Montreal write in an editorial accompanying the study that this approach could ultimately lead to new strategies for repairing and restoring cells lost to diseases or trauma in the hippocampus, and perhaps other regions of the brain.
But in an interview with WebMD, Goldman cautions that "it's a bit early in the game to think in practical terms of using these cells for transplantation purposes."
Among the problems that need to be tackled, Goldman says, are how best to deliver these cells to the brain and ensure that they will survive in sufficient numbers after transplant, and how to direct them to the parts of the brain where they will do the most good.
Many researchers think that memory impairment associated with aging is caused by damage to the hippocampus brought on by lifelong exposure to stress hormones. Several studies have shown that elderly people and rats with significant and prolonged elevation of these stress hormones have smaller hippocampal regions and show declines in memory due to damage to the hippocampus.
"It's a very interesting system," says Ronald McKay, PhD, chief of the laboratory of molecular biology at the National Institute of Neurological Disorders and Stroke. McKay, who has previously demonstrated that reducing stress hormone levels in aged rats can restore the production rate of brain cells in the hippocampus, reviewed the current study for WebMD.
"The hippocampus has these cells . which are replaced throughout life from dividing cells, so that whole process of division, . maturation and death seems to be going on all the time in this structure."
Although it's tempting to think that seed cells could be grown in the lab to restore cells damaged by neurodegenerative disorders such as Alzheimer's disease, much needs to be learned before such therapies are practical, Goldman and McKay say.
Instead, these precursor cells are likely to have their first uses in drug-testing labs, where researchers could explore whether specific drugs or combinations could be used to stimulate the growth of new brain cells within the hippocampus, Goldman says.
ELI5 if every cell in your body gets replaced over time, how does your brain maintain memories?
Neurons that compose memories do not normally die and are not replaced by newly forming cells. The cell is replaced in the sense that sooner or later every molecule is swapped out as a normal part of cellular maintenance but the entire cell is never replaced all at once.
Think of a car for example. A normal cell dying would be like a car exploding so you buy a new one. For neurons, its like replacing a wheel one day, the windshield the next, and the seats sometime after that. Sooner or later its a new car because the parts are replaced but it still operates the same and carries the same function.
Reminds me of the ship of Theseus thought experiment.
roughly speaking, the theory on the formation, and retention of memory is not so much about invdiudual cells, but the formation and maintenance of the links between cells in the brain. it is also possible that cellular behaviour (with reference to regeneration) in the brain is somewhat, or even radically different to the behaviour of cells in other tissues.
My knowledge of this is pretty peripheral, so feel free to correct me if anyone knows more. However, as I understand it, neurons do not replace themselves. They hang out in a special stage of the cell cycle that doesn't do any of the pre cell division stuff so they never undergo mitosis. Thus their positions in relation to each other don't change and you keep your memories. Also, I'm pretty sure this is why spinal cord injuries are so bad because the healthy nerve cells will never go through mitosis to replace the the damaged ones and the injury never really heals.
Well, AFAIK, almost no specific tissues undergo mitosis, our cells are replaced mostly from stem cells, with some degree of specialization (so, dermal stem cells is that - only dermal, and blood stem cells is only blood, they can't grow muscles or other type of tissues.
Problem with spinal cord damages mostly isn't that they can't divide and fill that gap, but because spinal neurons usually very very long, and once they're damaged, they can't grow correctly. Thus, even when research teams are able by some means to restore neural tissue in spinal cord, it takes long time to restore partial functionality and it's partial pretty much forever.
New neurons for life? Old people can still make fresh brain cells, study finds
One of the thorniest debates in neuroscience is whether people can make new neurons after their brains stop developing in adolescence—a process known as neurogenesis. Now, a new study finds that even people long past middle age can make fresh brain cells, and that past studies that failed to spot these newcomers may have used flawed methods.
The work “provides clear, definitive evidence that neurogenesis persists throughout life,” says Paul Frankland, a neuroscientist at the Hospital for Sick Children in Toronto, Canada. “For me, this puts the issue to bed.”
Researchers have long hoped that neurogenesis could help treat brain disorders like depression and Alzheimer’s disease. But last year, a study in Nature reported that the process peters out by adolescence, contradicting previous work that had found newborn neurons in older people using a variety of methods. The finding was deflating for neuroscientists like Frankland, who studies adult neurogenesis in the rodent hippocampus, a brain region involved in learning and memory. It “raised questions about the relevance of our work,” he says.
But there may have been problems with some of this earlier research. Last year’s Nature study, for example, looked for new neurons in 59 samples of human brain tissue, some of which came from brain banks where samples are often immersed in the fixative paraformaldehyde for months or even years. Over time, paraformaldehyde forms bonds between the components that make up neurons, turning the cells into a gel, says neuroscientist María Llorens-Martín of the Severo Ochoa Molecular Biology Center in Madrid. This makes it difficult for fluorescent antibodies to bind to the doublecortin (DCX) protein, which many scientists consider the “gold standard” marker of immature neurons, she says.
The number of cells that test positive for DCX in brain tissue declines sharply after just 48 hours in a paraformaldehyde bath, Llorens-Martín and her colleagues report today in Nature Medicine . After 6 months, detecting new neurons “is almost impossible,” she says.
When the researchers used a shorter fixation time—24 hours—to preserve donated brain tissue from 13 deceased adults, ranging in age from 43 to 87, they found tens of thousands of DCX-positive cells in the dentate gyrus, a curled sliver of tissue within the hippocampus that encodes memories of events. Under a microscope, the neurons had hallmarks of youth, Llorens-Martín says: smooth and plump, with simple, undeveloped branches.
In the sample from the youngest donor, who died at 43, the team found roughly 42,000 immature neurons per square millimeter of brain tissue. From the youngest to oldest donors, the number of apparent new neurons decreased by 30%—a trend that fits with previous studies in humans showing that adult neurogenesis declines with age. The team also showed that people with Alzheimer’s disease had 30% fewer immature neurons than healthy donors of the same age, and the more advanced the dementia, the fewer such cells.
Some scientists remain skeptical, including the authors of last year’s Nature paper. “While this study contains valuable data, we did not find the evidence for ongoing production of new neurons in the adult human hippocampus convincing,” says Shawn Sorrells, a neuroscientist at the University of Pittsburgh in Pennsylvania who co-authored the 2018 paper. One critique hinges on the DCX stain, which Sorrells says isn’t an adequate measure of young neurons because the DCX protein is also expressed in mature cells. That suggests the “new” neurons the team found were actually present since childhood, he says. The new study also found no evidence of pools of stem cells that could supply fresh neurons, he notes. What’s more, Sorrells says two of the brain samples he and his colleagues looked at were only fixed for 5 hours, yet they still couldn’t find evidence of young neurons in the hippocampus.
Llorens-Martín says her team used multiple other proteins associated with neuronal development to confirm that the DCX-positive cells were actually young, and were “very strict,” in their criteria for identifying young neurons.
Heather Cameron, a neuroscientist at the National Institute of Mental Health in Bethesda, Maryland, remains persuaded by the new work. Based on the “beauty of the data” in the new study, “I think we can all move forward pretty confidently in the knowledge that what we see in animals will be applicable in humans, she says. “Will this settle the debate? I’m not sure. Should it? Yes.”
How brain cells repair their DNA reveals “hot spots” of aging and disease
Salk scientists reveal new insights into neurodegenerative disorders and potential for genetic therapies
LA JOLLA—Neurons lack the ability to replicate their DNA, so they’re constantly working to repair damage to their genome. Now, a new study by Salk scientists finds that these repairs are not random, but instead focus on protecting certain genetic “hot spots” that appear to play a critical role in neural identity and function.
In this image of a neuron nucleus, bright spots show areas of focused genetic repair.
Click here for a high-resolution-image.
Credit: Salk Institute/Waitt Advanced Biophotonics Center
The findings, published in the April 2, 2021, issue of Science, give novel insights into the genetic structures involved in aging and neurodegeneration, and could point to the development of potential new therapies for diseases such Alzheimer’s, Parkinson’s and other age-related dementia disorders.
“This research shows for the first time that there are sections of genome that neurons prioritize when it comes to repair,” says Professor and Salk President Rusty Gage, the paper’s co-corresponding author. “We’re excited about the potential of these findings to change the way we view many age-related diseases of the nervous system and potentially explore DNA repair as a therapeutic approach.”
Unlike other cells, neurons generally don’t replace themselves over time, making them among the longest-living cells in the human body. Their longevity makes it even more important that they repair lesions in their DNA as they age, in order to maintain their function over the decades of a human life span. As they get older, neurons’ ability to make these genetic repairs declines, which could explain why people develop age-related neurodegenerative diseases like Alzheimer’s and Parkinson’s.
To investigate how neurons maintain genome health, the study authors developed a new technique they term Repair-seq. The team produced neurons from stem cells and fed them synthetic nucleosides—molecules that serve as building blocks for DNA. These artificial nucleosides could be found via DNA sequencing and imaged, showing where the neurons used them to make repairs to DNA that was damaged by normal cellular processes. While the scientists expected to see some prioritization, they were surprised by just how focused the neurons were on protecting certain sections of the genome.
“What we saw was incredibly sharp, well-defined regions of repair very focused areas that were substantially higher than background levels,” says co-first and co-corresponding author Dylan Reid, a former Salk postdoctoral scholar and now a fellow at Vertex Pharmaceutics. “The proteins that sit on these ‘hot spots’ are implicated in neurodegenerative disease, and the sites are also linked to aging.”
The authors found approximately 65,000 hot spots that covered around 2 percent of the neuronal genome. They then used proteomics approaches to detect what proteins were found at these hot spots, implicating many splicing-related proteins. (These are involved in the eventual production of other proteins.) Many of these sites appeared to be quite stable when the cells were treated with DNA-damaging agents, and the most stable DNA repair hot spots were found to be strongly associated with sites where chemical tags attach (“methylation”) that are best at predicting neuronal age.
From left: Rusty Gage and Dylan Reid
Click here for a high-resolution image.
Credit: Salk Institute, Dylan Reid
Previous research has focused on identifying the sections of DNA that suffer genetic damage, but this is the first time researchers have looked for where the genome is being heavily repaired.
“We flipped the paradigm from looking for damage to looking for repair, and that’s why we were able to find these hot spots,” Reid says. “This is really new biology that might eventually change how we understand neurons in the nervous system, and the more we understand that, the more we can look to develop therapies addressing age-related diseases.”
Gage, who holds the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Disease, adds, “Understanding which areas within the genome are vulnerable to damage is a very exciting topic for our lab. We think Repair-seq will be a powerful tool for research, and we continue to explore additional new methods to study genome integrity, particularly in relation to aging and disease.”
Other authors on the study are Patrick Reed, Ioana Nitulescu, Enoch Tsui, Jeffrey Jones, Claire McClain, Simon Schafer, Grace Chou, Tzu-Wen Wang, Nasun Hah, Sahaana Chandran and Jesse Dixon of Salk Johannes Schlachetzki, Addison Lana, and Christopher Glass of the University of California, San Diego Ake Lu and Steve Horvath of the University of California, Los Angeles.
The research was supported by the American Heart Association, the Paul G. Allen Frontiers Group, the JPB Foundation, the Dolby Foundation, the Helmsley Charitable Trust, and the National Institutes of Health.
Scientists discover brain cells that compete to sustain or suppress traumatic memories
Distinct clusters of neurons located in the amygdala modulate high and low fear states via connections to other regions in the brain. Kenta M. Hagihara, M.D., Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland (used with permission)
Two clusters of brain cells compete to promote either the persistence or disappearance of traumatic memories, according to a new study conducted in mice. The findings could provide important insights into human conditions such as post-traumatic stress disorder (PTSD), anxiety disorders, and associated problems such as alcohol use disorder (AUD) that can arise from the persistence of traumatic memories. The new research, led by scientists at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health, and their colleagues in Switzerland, is reported in the journal Nature.
“Over time, the distress of having experienced trauma will subside for some people, as memories of the trauma cease to provoke a fearful response,” says NIAAA Director Dr. George F. Koob. “For other people who have experienced trauma, however, the fearful memories persist, and can adversely affect their ability to engage in everyday activities. These fearful memories can continue even though a person may repeatedly encounter cues associated with a traumatic experience without a harm. The current study sheds light on the specific neural circuits that may underlie the persistence and the extinction of fearful memories associated with trauma.”
Scientists led by Andrew Holmes, Ph.D., chief of NIAAA’s Laboratory of Behavioral and Genomic Neuroscience, examined clusters of neurons, known as intercalated cells or ITCs, that are packed tightly around the mouse amygdala. Found deep within the temporal lobes of mammals’ brains, the amygdala is well-known as a hub for processing emotions. It is therefore a likely actor in the brain systems that underlie the formation of fearful memories associated with certain environmental cues and the successful extinction of those memories when the same cues later predict no harm.
In a series of behavioral in vivo brain imaging and neurophysiology studies, NIAAA scientists collaborated with researchers in the United States, Switzerland and Germany to assess the potential roles of ITCs as mice learned to associate a cue (e.g., a sound) with a foot-shock (a fear-inducing event), and then extinguished the association by no longer pairing the cue with a foot-shock.
The researchers found that two distinct ITC clusters promote either a fear response or extinction of the cue / foot-shock association. They further revealed that the clusters effectively compete with one another, through a process known as mutual synaptic inhibition, to determine the relative strength of each memory and, hence, the level of defensive behavior shown by the animal. The study also showed that the ITC clusters have long-range connections to known fear-regulating regions in the midbrain and prefrontal cortex.
“The persistence of disturbing memories of a traumatic event are one of the hallmarks of PTSD and some anxiety disorders,” says Dr. Holmes. “Our findings identify a neural circuit within the amygdala that orchestrates activity across a broad brain network to exert a powerful influence over the ability to switch between high and low fear states. This finding now raises interesting questions about whether dysfunction of this brain system could contribute to the marked individual differences in risk for trauma-related psychiatric disorders.”
Discovery of extremely long-lived proteins may provide insight into cell aging and neurodegenerative diseases
Salk researchers find that the adult brain contains proteins that last a lifetime
LA JOLLA, CA—One of the big mysteries in biology is why cells age. Now scientists at the Salk Institute for Biological Studies report that they have discovered a weakness in a component of brain cells that may explain how the aging process occurs in the brain.
The scientists discovered that certain proteins, called extremely long-lived proteins (ELLPs), which are found on the surface of the nucleus of neurons, have a remarkably long lifespan.
While the lifespan of most proteins totals two days or less, the Salk
Institute researchers identified ELLPs in the rat brain that were as old
as the organism, a finding they reported in Science.
The Salk scientists are the first to discover an essential intracellular machine whose components include proteins of this age. Their results suggest the proteins last an entire lifetime, without being replaced.
ELLPs make up the transport channels on the surface of the nucleus gates that control what materials enter and exit. Their long lifespan might be an advantage if not for the wear-and-tear that these proteins experience over time. Unlike other proteins in the body, ELLPs are not replaced when they incur aberrant chemical modifications and other damage.
Damage to the ELLPs weakens the ability of the three-dimensional transport channels that are composed of these proteins to safeguard the cell’s nucleus from toxins, says Martin Hetzer, a professor in Salk’s Molecular and Cell Biology Laboratory, who headed the research. These toxins may alter the cell’s DNA and thereby the activity of genes, resulting in cellular aging.
Funded by the Ellison Medical Foundation and the Glenn Foundation for Medical Research, Hetzer’s research group is the only lab in the world that is investigating the role of these transport channels, called the nuclear pore complex (NPC), in the aging process.
This microscope image shows extremely long-lived proteins, or ELLPs, glowing green on the outside of the nucleus of a rat brain cell. DNA inside the nucleus is pictured in blue.
The Salk scientists discovered that the ELLPs, which form channels through the wall of the nucleus, lasted for more than a year without being replaced. Deterioration of these proteins may allow toxins to enter the nucleus, resulting in cellular aging.
Image: Courtesy of Brandon Toyama, Salk Institute for Biological Studies
Previous studies have revealed that alterations in gene expression underlie the aging process. But, until the Hetzer lab’s discovery that mammals’ NPCs possess an Achilles’ heel that allows DNA-damaging toxins to enter the nucleus, the scientific community has had few solid clues about how these gene alterations occur.
“The fundamental defining feature of aging is an overall decline in the functional capacity of various organs such as the heart and the brain,” says Hetzer. “This decline results from deterioration of the homeostasis, or internal stability, within the constituent cells of those organs. Recent research in several laboratories has linked breakdown of protein homeostasis to declining cell function.”
The results that Hetzer and his team report today suggest that declining neuron function may originate in ELLPs that deteriorate as a result of damage over time.
“Most cells, but not neurons, combat functional deterioration of their protein components through the process of protein turnover, in which the potentially impaired parts of the proteins are replaced with new functional copies,” says Hetzer.
“Our results also suggest that nuclear pore deterioration might be a general aging mechanism leading to age-related defects in nuclear function, such as the loss of youthful gene expression programs,” he adds.
The findings may prove relevant to understanding the molecular origins of aging and such neurodegenerative disorders as Alzheimer’s disease and Parkinson’s disease.
In previous studies, Hetzer and his team discovered large filaments in the nuclei of neurons of old mice and rats, whose origins they traced to the cytoplasm. Such filaments have been linked to various neurological disorders including Parkinson’s disease. Whether the misplaced molecules are a cause, or a result, of the disease has not yet been determined.
Also in previous studies, Hetzer and his team documented age-dependent declines in the functioning of NPCs in the neurons of healthy aging rats, which are laboratory models of human biology.
Hetzer’s team includes his colleagues at the Salk Institute as well as John Yates III, a professor in the Department of Chemical Physiology of The Scripps Research Institute. The co-first authors on the study were Brandon H. Toyama, a postdoctoral researcher in Hetzer’s laboratory, and Jeffrey N. Savas, a postdoctoral researcher in Yates’ laboratory.
When Hetzer decided three years ago to investigate whether the NPC plays a role in initiating or contributing to the onset of aging and certain neurodegenerative diseases, some members of the scientific community warned him that such a study was too bold and would be difficult and expensive to conduct. But Hetzer was determined despite the warnings.
He adds that without foundation funding, the study would not have progressed to the point that its findings are published in a leading journal.
About the Salk Institute for Biological Studies:
The Salk Institute for Biological Studies is one of the world’s preeminent basic research institutions, where internationally renowned faculty probe fundamental life science questions in a unique, collaborative, and creative environment. Focused both on discovery and on mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer’s, diabetes and infectious diseases by studying neuroscience, genetics, cell and plant biology, and related disciplines.
Faculty achievements have been recognized with numerous honors, including Nobel Prizes and memberships in the National Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas Salk, M.D., the Institute is an independent nonprofit organization and architectural landmark.
For more information:
Authors: Jeffrey N. Savas, Brandon H. Toyama, Tao Xu, John R. Yates and Martin W. Hetzer
Extremely Long-Lived Nuclear Pore Proteins in the Rat Brain
Does your body really replace itself every seven years?
Know yourself love yourself be true to yourself. These old adages have been batted around throughout the years by a whole cross section of artists, entertainers and philosophical types, from John Paul Sartre ("We only become what we are by the radical and deep-seated refusal of that which others have made of us") to Bob Dylan ("If you try to be anyone but yourself, you will fail") to Katharine Hepburn ("If you always do what interests you at least one person is pleased").
But how do you get to know yourself when you are constantly changing? Whether it's shedding skin, renewing the lungs or growing new hairs, the human body is in constant flux.
According to researchers, the body replaces itself with a largely new set of cells every seven years to 10 years, and some of our most important parts are revamped even more rapidly [sources: Stanford University, Northrup].
Some of you may be thinking, "Well, that explains why my spouse/sibling/parent/co-worker acts like a little kid." Others might be expecting those new cells to be the key to a longer life. Unfortunately, it's a little more complicated than that.
In the early '50s, researchers discovered the body's rejuvenating power by – yes, really – feeding and injecting subjects with radioactive atoms and observing their movement. They found that, on average, 98 percent of the That explains why our skin flakes off, our nails grow and our hair falls out. But if we are constantly being filled with brand-spanking-new cells, why is it that the body grows old? Shouldn't, this influx of new cells be like a shot of Botox? When it comes to aging, it appears that the secret lies not in our cells but, more specifically, in the cellular DNA [source: Wade].]atoms inside the body – the smallest units of matter, which form the molecules that help comprise bodily cells – are replaced each year. Most new atoms are taken in through the air we breathe, the food we eat and the liquids we drink [source: NPR].
More than five decades later, Swedish molecular biologist Dr. Jonas Frisen studied body tissue renewal by measuring levels of a radioactive material called carbon-14. This material was released in the air before testing nuclear weapons aboveground was banned in 1963. Carbon-14 is breathed in by plants, which humans and animals eat every day, and is part of our DNA. But unlike other atoms and molecules that are constantly changing, a person's DNA remains the same from the day of a cell's birth – which occurs when a parent cell divides – throughout its life span. When a cell divides, in other words, the DNA incorporated in the new cell includes a certain level of carbon-14 that corresponds to the level of the material in the air around us at the time. This serves as a time stamp of sorts, by which researchers can determine when the cell was created based on the level of carbon-14 in its DNA [sources: Wade, Science Update].
What Frisen found is that the body's cells largely replace themselves every 7 to 10 years. In other words, old cells mostly die and are replaced by new ones during this time span. The cell renewal process happens more quickly in certain parts of the body, but head-to-toe rejuvenation can take up to a decade or so.
That explains why our skin flakes off, our nails grow and our hair falls out. But if we are constantly being filled with brand-spanking-new cells, why is it that the body grows old? Shouldn't this influx of new cells be like a shot of Botox? When it comes to aging, it appears that the secret lies not in our cells but, more specifically, in the cellular DNA [source: Wade].
Doctors and scientists think that various cancers grow in the human body when cancerous cells self-replenish through division. But one of the most common forms of treatment, chemotherapy, works by wiping out a wide range of cells indiscriminately, without focusing particularly on those that are the source of the cancer. By learning how and when cells self-renew, researchers hope to be able to pinpoint cancer originators and block those cells from duplicating without interfering with other healthy cells [source: Stanford].
The body renews itself at varying paces. Just how long the cells in certain areas last depends on how much work they're asked to do. Red blood cells, for example, enjoy a quick life span of only about four months as a result of their arduous journey through the circulatory system, carting oxygen to tissues throughout the body [source: Wade].
Here are the life expectancies for other cells [sources: Wade, Epstein]:
Skin: The epidermis sees a fair amount of wear and tear, thanks to its role as the body's outermost layer of protection. These skin cells rejuvenate every two to four weeks.
Hair: The body's natural fuzz has a life span of about six years for women and three years for men.
Liver: The liver is the human body's detoxifier, purifying a wide variety of contaminants from our systems. It's aided in the process by a constant blood supply and remains largely immune to damage from these toxins by renewing itself with new cells every 150 to 500 days.
Stomach and Intestines: Cells that line the surface of the stomach and intestines have a difficult, short life. Constantly battered by corrosives like stomach acids, they typically last only up to five days.
Bones: Cells in the skeletal system regenerate almost constantly, but the complete process takes a full 10 years. The renewal process slows down as we age, so our bones get thinner.
Despite all this regeneration all the time, people who want to live forever shouldn't give up on that search for the fountain of youth. The truth is that we still get old and we still die. Frisen and others believe that this may be because of DNA mutations, which worsen as they're passed along to new cells over time [sources: Wade, Epstein].
There are also some cells that never leave us and may aid the aging process, or at least the body's breakdown over time. While the eye's cornea can regenerate itself in as little as one day, the lens and other areas don't change. Similarly, neurons in the cerebral cortex – the brain's outside layer that governs memory, thought, language, attention and consciousness – stay with us from birth to death. Because they aren't replaced, the loss of these cells over time can cause maladies like dementia. The good news is that other areas of the brain, like the olfactory bulb that helps us smell and the hippocampus that helps us learn, can and do rejuvenate [sources: Wade, Epstein].
So get out there and show off that big ol' brain like a clever version of a "Baywatch" lifeguard. It's one asset that won't last forever.
Are brain cells replaced over time? - Biology
Science has come a long way in helping us understand the way the brain changes in addiction. In this section, we will provide updates of current research on addiction, recovery, and the brain.
3 Key Points to Understand the Brain and Addiction:
1. Some characteristics of addiction are similar to other chronic diseases.
Just as cardiovascular disease damages the heart and changes its functioning, addiction changes the brain and impairs the way it works. Below is an image of the brain (left) and the heart (right).
These images show how scientists can use imaging technology to measure functioning of the brain and heart. Greater activity is shown in reds and yellows, and reduced activity is shown in blues and purples. Both the healthy brain and the healthy heart show greater activity than the diseased brain and heart, because both addiction and heart disease cause changes in function. In drug addiction, the frontal cortex in particular shows less activity. This is the part of the brain associated with judgment and decision-making (NIDA).
Addiction is similar to other chronic diseases in the following ways:
- It is preventable
- It is treatable
- It changes biology
- If untreated, it can last a lifetime
2. Substances of misuse trick the brain’s reward system.
The brain can experience pleasure from all sorts of things we like to do in life eat a piece of cake, have a sexual encounter, play a video game. The way the brain signals pleasure is through the release of a neurotransmitter (a chemical messenger) called dopamine into the nucleus accumbens, the brain’s pleasure center. This is generally a good thing it ensures that people will seek out things needed for survival. But drugs of misuse, such as nicotine, alcohol, and heroin, also cause the release of dopamine in the nucleus accumbens, and in some cases these drugs cause much more dopamine release than natural, non-drug rewards.
Below is a picture (helpguide.org) of the brain and the nucleus accumbens, in addition to some other brain regions that are affected by addition.
The brain’s nucleus accumbens activated by alcohol (Gilman et al., 2008)
Addictive drugs can provide a shortcut to the brain’s reward system by flooding the nucleus accumbens with dopamine. Additionally, addictive drugs can release 2 to 10 times the amount of dopamine that natural rewards do, and they do it more quickly and reliably.
Over time, drugs become less rewarding, and craving for the drug takes over. The brain adapts to the effects of the drug (an effect known as tolerance), and because of these brain adaptations, dopamine has less impact. People who develop an addiction find that the drug no longer gives them as much pleasure as it used to, and that they have to take greater amounts of the drug more frequently to feel high.
There is a distinction between liking and wanting the drug over time, the liking decreases and the wanting increases. Individuals with a substance use disorder continue to seek and use the substance, despite the negative consequences and tremendous problems caused for themselves and for their loved ones, because the substance allows them to simply feel normal.
3. The brain can recover – but it takes time!
How the brain recovers from addiction is an exciting and emerging area of research. There is evidence that the brain does recover the image below shows the healthy brain on the left, and the brain of a patient who misused methamphetamine in the center and the right. In the center, after one month of abstinence, the brain looks quite different than the healthy brain however, after 14 months of abstinence, the dopamine transporter levels (DAT) in the reward region of the brain (an indicator of dopamine system function) return to nearly normal function (Volkow et al., 2001).
There is limited research on the brain’s recovery from alcohol and marijuana use. However, recent studies have shown that some recovery does take place. For example, one study found that adolescents that became abstinent from alcohol had significant recovery with respect to behavioral disinhibition and negative emotionality (Hicks et al., 2012). Lisdahl and colleagues propose that this could mean that some recovery is occurring in the prefrontal cortex after a period of abstinence. Furthermore, other research has found that number of days abstinent from alcohol was associated with improved executive functioning, larger cerebellar volumes, and improved short-term memory.
While promising, this field of research is in its infancy and there have been conflicting results that instead show minimal to no recovery from cognitive deficits. This is especially true for studies evaluating the brain’s recovery from marijuana use, specifically in regards to IQ. On the other hand, some studies have shown that former marijuana users demonstrate increased activation in parts of the brain associated with executive control and attention. Whether this is associated with the compensatory response or brain recovery has yet to be determined.
What is clear is that alcohol and marijuana do have neurotoxic effects and that, to some degree, this damage can be reversed. There is minimal evidence on how we can improve brain recovery from substance use, but emerging literature suggests that exercise as an intervention may improve brain recovery. Physical activity has been shown to improve brain health and neuroplasticity. In previous studies of adults, physical activity has improved executive control, cerebral blood flow, and white matter integrity. While none of these interventions have been done in adolescent alcohol or marijuana users, this approach is promising and should be investigated further.
The Top Tools Being Utilized for Research on the Brain in Recovery
Functional brain measurement techniques:
Methods that provide dynamic physiological information about brain function/activity. Functional imaging techniques allow scientists to measure the contributions of various structures to specific psychological processes (e.g., attention, working memory, etc.). Commonly obtained while participants complete ‘tasks’, functional images offer insight to the brain regions that are activated, or recruited, to perform a given task. Atypical brain function in patient populations can include reduced neural activation or a different pattern of brain activation as compared to healthy control populations.
Functional Magnetic Resonance Imaging (fMRI)
Also known as a functional MRI (fMRI), this imaging technique measures brain activity by detecting changes associated with blood flow and oxygenation.
- Numerous studies utilizing functional magnetic resonance imaging (fMRI) have shown that drug cues elicit increased regional blood flow in reward-related brain areas among addicted participants that is not found among normal controls (Bunce et al., 2013)
See the fMRI in action:
An electroencephalogram (EEG) is a test that detects electrical activity and patterns in the brain using small, flat, non-invasive metal discs (electrodes) attached to the scalp. Brain cells communicate continuously via electrical impulses, even when asleep, and this activity is reflected via fluctuating lines on an EEG recording.
See the EEG in action:
Functional Near infrared spectroscopy (fNIRS)
Imaging technique that monitors changes in oxygenation concentrations during neural activities by measuring the differing absorption levels of near-infrared light (NIR) between the spectrum of 700-900 millimeters.
See the fNIRS in action:
Positron Emission Tomography (PET)
Nuclear imaging technique that uses a radioactive drug tracer to detect how tissues and organs are functioning, measuring low concentrations of molecules to detect cell-to-cell communication, and track a substances distribution within and movement into and out of the brain.
See the PET in action:
PET SCAN: The right scan is the brain of an individual with chronic cocaine use disorder. Compared to the control on the left, the PET image on the right has less red, indicating that the brain of the individual with cocaine use disorder has less glucose and is less active. Lower activity in the brain disrupts many of the brain's normal functions.
Structural brain measurement techniques:
Imaging techniques that allow one to examine the brain’s anatomical structure. Structural imaging provides static information, and is analogous to taking a photograph of the brain. These images permit evaluation of gross anatomical abnormalities, including tissue atrophy (i.e., loss of neural tissue) and reduced white matter integrity (i.e., weakened connections between neural structures).
Magnetic Resonance Imaging (MRI)
Imaging technique that uses a magnetic field and radio waves to generate detailed images of water molecules in a cross section or area of the brain. Different types of tissue hold different amounts of water, generating maps or pictures of the brain that contrast and detect structural abnormalities such as size, density, and volume of brain tissue such as white and grey matter.
See the MRI in action:
Diffusion Tensor Imaging (DTI)
MRI-based neuroimaging technique that detects microstructural changes or diseases of the nervous system tissue (neuropathology), characterizing the location and orientation of white matter tracts through the generation of brain maps that use contrasting colors to reveal an image that highlights the diffusion of water molecules.
See the DTI in action:
Limitations of brain measurement tools for addiction research:
- High cost of utilizing the technologies within research studies.
- Some neuroimaging techniques require IV injection of a radioactive tracer (e.g., PET scan).
- Some techniques are not suitable for everyone. For example, individuals with metal implants and pacemakers cannot undergo magnetic resonance imaging given the nature with which this image is obtained.
- Research methods must be tailored to imaging requirements. fMRI, for example, is sensitive to physical movement and requires that the individual being scanned remain as still as possible. Therefore, tasks performed during an fMRI scan must not require excessive movement for successful performance.
- Different imaging techniques have varying advantages/disadvantages. Some methods provide better temporal resolution (the accuracy of capturing an image with respect to time), whereas others provide superior spatial resolution (the visual clarity of the image). Although no single technique has perfect spatial and temporal resolution, multimodal imaging techniques (the simultaneous use of 2 or more techniques) are being more commonly implemented and provide a more complete picture of brain structure/function.
What happens to the brain as we age?
Brain aging is inevitable to some extent, but it is not uniform it affects everyone, or every brain, differently.
Share on Pinterest The effects of aging on the brain can vary from person to person.
Slowing down brain aging or stopping it altogether would be the ultimate elixir to achieve eternal youth. Is brain aging a slippery slope that we need to accept? Or are there steps that we can take to reduce the rate of decline?
At around 3 pounds in weight, the human brain is a staggering feat of engineering, with around 100 billion neurons interconnected via trillions of synapses.
Throughout a lifetime, the brain changes more than any other part of the body. From the moment the brain begins to develop in the third week of gestation to old age, its complex structures and functions are changing, networks and pathways connecting and severing.
During the first few years of life, the brain forms more than 1 million new neural connections every second. The size of the brain increases fourfold in the preschool period, and by age 6, it reaches around 90% of its adult volume.
The frontal lobes are the area of the brain responsible for executive functions, such as planning, working memory, and impulse control. These are among the last areas of the brain to mature, and they may not develop fully until around 35 years of age .
As people age, their bodily systems — including the brain — gradually decline. “Slips of the mind” are associated with getting older. That said, people often experience those same slight memory lapses in their 20s but do not give it a second thought.
Older adults often become anxious about memory slips due to the link between impaired memory and Alzheimer’s disease. However, Alzheimer’s and other dementias are not a part of the normal aging process.
Common memory changes that are associated with normal aging include:
- Difficulty learning something new: Committing new information to memory can take longer.
- Multitasking: Slowed processing can make planning parallel tasks more difficult.
- Recalling names and numbers: Strategic memory, which helps with remembering names and numbers, begins to decline at age 20.
- Remembering appointments: Without cues to recall the information, the brain may put appointments into “storage” and not access them unless something jogs the person’s memory.
Although some studies show that one-third of older adults struggle with declarative memory — that is, memories of facts or events that the brain has stored and can retrieve — other studies indicate that one-fifth of 70-year-olds perform cognitive tests just as well as people aged 20.
Scientists are currently piecing together sections of the giant puzzle of brain research to determine how the brain subtly alters over time to cause these changes.
General changes that researchers think occur during brain aging include:
- Brain mass: Shrinkage in the frontal lobe and hippocampus, which are areas involved in higher cognitive function and encoding new memories, starts at around the age of 60 or 70 years.
- Cortical density: This refers to the thinning of the outer-ridged surface of the brain due to declining synaptic connections. Fewer connections may contribute to slower cognitive processing.
- White matter: White matter consists of myelinated nerve fibers that are bundled into tracts and carry nerve signals between brain cells. Researchers think that myelin shrinks with age, and, as a result, processing is slower and cognitive function is reduced.
- Neurotransmitter systems: Researchers suggest that the brain generates fewer chemical messengers with age, and it is this decrease in dopamine, acetylcholine, serotonin, and norepinephrine activity that may play a role in declining cognition and memory and increasing depression.
In understanding the neural basis of cognitive decline, researchers can uncover which therapies or strategies may help slow or prevent brain deterioration.
Several brain studies are ongoing to solve the brain aging conundrum, and scientists are frequently making discoveries.
The sections below will outline some of these in more detail.
In 2017, researchers from Albert Einstein College of Medicine in New York City, NY, revealed in a mouse study that stem cells in the brain’s hypothalamus likely control how fast aging occurs in the body.
“Our research shows that the number of hypothalamic neural stem cells naturally declines over the life of the animal, and this decline accelerates aging,” says Dr. Dongsheng Cai, a professor of molecular pharmacology.
“But,” he adds, “we also found that the effects of this loss are not irreversible. By replenishing these stem cells or the molecules they produce, it’s possible to slow and even reverse various aspects of aging throughout the body.”
Injecting hypothalamic stem cells into the brains of normal old and middle-aged mice, whose stem cells had been destroyed, slowed or reversed measures of aging. The researchers say that this is a first step toward slowing the aging process and potentially treated age-related conditions.
“SuperAgers” are a rare group of individuals over the age of 80 years who have memories as sharp as those of healthy people decades younger.
Research by scientists at Northwestern University Feinberg School of Medicine in Chicago, IL, compared SuperAgers with a control group of same-age individuals.
They found that the brains of the SuperAgers shrink at a slower rate than those of their age-matched peers, which results in a greater resistance to the typical memory loss that occurs age. This suggests that age-related cognitive decline is not inevitable.
“We found that SuperAgers are resistant to the normal rate of decline that we see in average [older adults], and they’re managing to strike a balance between life span and health span, really living well and enjoying their later years of life,” says Emily Rogalski, an associate professor.
By studying how SuperAgers are unique, the researchers hope to unearth biological factors that might contribute to maintaining memory ability in advanced age.
Researchers have discovered several factors that speed up brain aging.
For example, obesity in midlife may accelerate brain aging by around 10 years, and both sugar and diet varieties of soda are associated with poorer brain health.
A growing body of evidence suggests that people who experience the least declines in cognition and memory all share certain habits:
- engaging in regular physical activity
- pursuing intellectually stimulating activities
- staying socially active
- managing stress
- eating a healthful diet
- sleeping well
Recent research highlights a plethora of ways that people can actively take charge of their health and perhaps decrease the rate at which their brains age.
The following sections will look at some of these tips in more detail.
One intervention that crops up time and time again to stave off age-related mental decline is physical exercise.
Performing a combination of aerobic and resistance exercise of moderate intensity for at least 45 minutes each session on as many days of the week as possible can significantly boost brain power in people aged 50 and over.
Likewise, other research by the University of Miami in Florida found that individuals over the age of 50 who engaged in little to no exercise experienced a decline in memory and thinking skills comparable to 10 years of aging in 5 years, compared with those who took part in moderate or high intensity exercise.
Essentially, physical activity slowed brain aging by 10 years.
Dancing may also have an anti-aging effect on the brains of older adults. A study by the German Center for Neurodegenerative Diseases in Magdeburg found that although regular exercise can reverse the signs of brain aging, the most profound effect was among people who danced.
Playing an instrument
Researchers at Baycrest Health Sciences in Toronto, Canada, revealed why playing a musical instrument may help older adults ward off age-related cognitive decline and retain their listening skills.
Researchers found that learning to play a sound on a musical instrument changes brain waves in such a way that improves an individual’s listening and hearing skills. The alteration in brain activity indicates that the brain rewires itself to compensate for disease or injuries that might prevent a person’s ability to perform tasks.
“It has been hypothesized,” says Dr. Bernhard Ross, a senior scientist at Baycrest’s Rotman Research Institute, “that the act of playing music requires many brain systems to work together, such as the hearing, motor, and perception systems.”
“This study was the first time we saw direct changes in the brain after one session, demonstrating that the action of creating music leads to a strong change in brain activity,” he adds.
Eating a healthful diet
A key component of brain health is diet. In 2018, researchers linked omega-3 and omega-6 fatty acids in the blood with healthy brain aging.
Another study has also determined that consuming foods included in the Mediterranean or MIND diet is associated with a lower risk of memory difficulties in older adults.
Research by the University of Illinois at Urbana-Champaign discovered that middle-aged people with higher levels of lutein — which is a nutrient present in green leafy vegetables, such as kale and spinach, as well as eggs and avocados — had similar neural responses to younger individuals than those of people of the same age.
“As people get older, they experience typical decline. However, research has shown that this process can start earlier than expected. You can even start to see some differences in the 30s,” says first study author Anne Walk, a postdoctoral scholar.
“We want to understand how diet impacts cognition throughout the life span,” she adds. “If lutein can protect against decline, we should encourage people to consume lutein-rich foods at a point in their lives when it has maximum benefit.”
The number of adults in the United States over the age of 65 is set to more than double in the next 40 years, rising from 40.2 million in 2010 to 88.5 million by 2050.
Due to this aging population, it will become increasingly important to understand the cognitive changes that go hand in hand with aging.
Although many questions remain regarding the aging brain, research is making progress in illuminating what happens to our cognitive functions and memory throughout our lifetime.
It is also emphasizing the ways in which we can preserve our mental abilities to improve our quality of life as we advance into older adulthood.