Posts tagged fruit flies
Articles and news from the latest research reports.
Prions can be notoriously destructive, spurring proteins to misfold and interfere with cellular function as they spread without control. New research, published in the open access journal PLOS Biology on February 11, 2014, from scientists at the Stowers Institute for Medical Research reveals that certain prion-like proteins, however, can be precisely controlled so that they are generated only in a specific time and place. These prion-like proteins are not involved in disease processes; rather, they are essential for creating and maintaining long-term memories.
“This protein is not toxic; it’s important for memory to persist,” says Stowers researcher Kausik Si, Ph.D., who led the study. To ensure that long-lasting memories are created only in the appropriate neural circuits, Si explains, the protein must be tightly regulated so that it adopts its prion-like form only in response to specific stimuli. He and his colleagues report on the biochemical changes that make that precision possible.
Si’s lab is focused on finding the molecular alterations that encode a memory in specific neurons as it endures for the days, months, or years—even as the cells’ proteins are degraded and renewed. Increasingly, their research is pointing toward prion-like proteins as critical regulators of long-term memory.
In 2012, Si’s group demonstrated that prion formation in nerve cells is essential for the persistence of long-term memory in fruit flies. Prions are a fitting candidate for this job because their conversion is self-sustaining: once a prion-forming protein has shifted into its prion shape, additional proteins continue to convert without any additional stimulus.
Si’s team found that in fruit flies, the prion-forming protein Orb2 is necessary for memories to persist. Flies that produce a mutated version of Orb2 that is unable to form prions learn new behaviors, but their memories are short-lived. “Beyond a day, the memories become unstable. By three days, the memory has completely disappeared,” Si explains.
In the new study, Si wanted to find out how this process could be controlled so that memories form at the right time. “We know that all experiences do not form long-term memory—somehow the nervous system has a way to discriminate. So if prion-formation is the biochemical basis of memory, it must be regulated.” Si says. “But prion formation appears to be random for all the cases we know of so far.”
Si and his colleagues knew that Orb2 existed in two forms—Orb2A and Orb2B. Orb2B is widespread throughout the fruit fly’s nervous system, but Orb2A appears only in a few neurons, at extremely low concentrations. What’s more, once it is produced, Orb2A quickly falls apart; the protein has a half-life of only about an hour.
“When Orb2A binds to the more abundant form, it triggers conversion to the prion state, acting as a seed for the conversion. Once conversion begins, it is a self-sustaining process; additional Orb2 continues to convert to the prion state, with or without Orb2A. By altering the abundance of the Orb2A seed”, Si says, “cells might regulate where, when, and how the conversion process is engaged”. But how do nerve cells control the abundance of the Orb2A seed?
Their experiments revealed that when a protein called TOB associates with Orb2A , it becomes much more stable, with a new half-life of 24 hours. This step increases the prevalence of the prion-like state and explains how Orb2’s conversion to the prion state can be confined in both time and space.
The findings raise a host of new questions for Si, who now wants to understand what happens when Orb2 enters its prion-like state, as well as where in the brain the process occurs. While unraveling these mechanisms will likely be more accessible in the fruit fly than in more complex organisms, Si points out that proteins related to Orb2 and TOB have also been found in the brains of mice and humans. He has already shown that in the sea snail Aplysia, conversion to a prion-like state facilitates long-term change in synaptic strength. “This basic mechanism appears to be conserved across species,” he notes.
Finding could explain age-related decline in motor function
Scientists from the School of Medicine at The University of Texas Health Science Center at San Antonio have found a clue as to why muscles weaken with age. In a study published today in The Journal of Neuroscience, they report the first evidence that “set points” in the nervous system are not inalterably determined during development but instead can be reset with age. They observed a change in set point that resulted in significantly diminished motor function in aging fruit flies.
“The body has a set point for temperature (98.6 degrees), a set point for salt level in the blood, and other homeostatic (steady-state) set points that are important for maintaining stable functions throughout life,” said study senior author Ben Eaton, Ph.D., assistant professor of physiology at the Health Science Center. “Evidence also points to the existence of set points in the nervous system, but it has never been observed that they change, until now.”
Dr. Eaton and lead author Rebekah Mahoney, a graduate student, recorded changes in the neuromuscular junction synapses of aging fruit flies. These synapses are spaces where neurons exchange electrical signals to enable motor functions such as walking and smiling. “We observed a change in the synapse, indicating that the homeostatic mechanism had adjusted to maintain a new set point in the older animal,” Mahoney said.
The change was nearly 200 percent, and the researchers predicted that it would leave muscles more vulnerable to exhaustion.
Aside from impairing movement in aging animals, a new functional set point in neuromuscular junctions could put the synapse at risk for developing neurodegeneration — the hallmark of disorders such as Alzheimer’s and Parkinson’s diseases, Mahoney said.
“Observing a change in the set point in synapses alters our paradigms about how we think age affects the function of the nervous system,” she said.
It appears that a similar change could lead to effects on learning and memory in old age. An understanding of this phenomenon would be invaluable and could lead to development of novel therapies for those issues, as well.
(Source: uthscsa.edu)
New Sleep Gene, Redeye, Discovered in Fruitflies Promotes the Need to Sleep
All creatures great and small, including fruitflies, need sleep. Researchers have surmised that sleep – in any species — is necessary for repairing proteins, consolidating memories, and removing wastes from cells. But, really, sleep is still a great mystery.
Image caption: An alpha subunit of the nicotinic acetylcholine receptor accounts for the rye mutant phenotype. Expression pattern of redeye (green). Credit: Amita Sehgal and Mi Shi, PhD, Perelman School of Medicine, University of Pennsylvania
The timing of when we sleep versus are awake is controlled by cells in tune with circadian rhythms of light and dark. Most of the molecular components of that internal clock have been worked out. On the other hand, how much we sleep is regulated by another process called sleep homeostasis, however little is known about its molecular basis.
In a study published in eLIFE, Amita Sehgal, PhD, professor of Neuroscience at the Perelman School of Medicine, University of Pennsylvania, and colleagues, report a new protein involved in the homeostatic regulation of sleep in the fruitfly, Drosophila. Sehgal is also an investigator with the Howard Hughes Medical Institute (HHMI).
The researchers conducted a screen of mutant flies to identify short-sleeping individuals and found one, which they dubbed redeye. These mutants show a severe reduction in the amount of time they slumber, sleeping only half as long as normal flies. While the redeye mutants were able to fall asleep, they would wake again in only a few minutes.
The team found that the redeye gene encodes a subunit of the nicotinic acetylcholine receptor. This type of acetylcholine receptor consists of multiple protein subunits, which form an ion channel in the cell membrane, and, as the name implies, also binds to nicotine. Although acetylcholine signaling — and cigarette smoking — typically promote wakefulness, the particular subunit studied in the eLIFE paper is required for sleep in Drosophila.
Levels of the redeye protein in the fly oscillate with the cycles of light and dark and peak at times of daily sleep. Normally, the redeye protein is expressed at times of increasing sleep need in the fly, right around the afternoon siesta and at the time of night-time sleep. From this, the team concluded that the redeye protein promotes sleep and is a marker for sleepiness – suggesting that redeye signals an acute need for sleep, and then helps to maintain sleep once it is underway.
In addition, cycling of the redeye protein is independent of the circadian clock in normal day:night cycles, but depends on the sleep homeostat. The team concluded this because redeye protein levels are upregulated in short-sleeping mutants as well as in wild-type animals following sleep deprivation. And, mutant flies had normal circadian rhythms, suggesting that their sleep problems were the result of disrupted sleep/wake homeostasis.
Ultimately the team wants to use the redeye gene to locate sleep homeostat neurons in the brain. “We propose that the homeostatic drive to sleep increases levels of the redeye protein, which responds to this drive by promoting sleep,” says Sehgal. Identification of molecules that reflect sleep drive could lead to the development of biomarkers for sleep, and may get us closer to revealing the mystery of the sleep homeostat.
(Source: uphs.upenn.edu)
Fighting Flies
When one encounters a group of fruit flies invading their kitchen, it probably appears as if the whole group is vying for a sweet treat. But a closer look would likely reveal the male flies in the group are putting up more of a fight, particularly if ripe fruit or female flies are present. According to the latest studies from the fly laboratory of California Institute of Technology (Caltech) biologist David Anderson, male Drosophilae, commonly known as fruit flies, fight more than their female counterparts because they have special cells in their brains that promote fighting. These cells appear to be absent in the brains of female fruit flies.
"The sex-specific cells that we identified exert their effects on fighting by releasing a particular type of neuropeptide, or hormone, that has also been implicated in aggression in mammals including mouse and rat," says Anderson, the Seymour Benzer Professor of Biology at Caltech, and corresponding author of the study. "In addition, there are some recent papers implicating increased levels of this hormone in people with personality disorders that lead to higher levels of aggression."
The team’s findings are outlined in the January 16 version of the journal Cell.
Discoveries in How Memories Form Could Help Treat Dementia
Do fruit flies hold the key to treating dementia? Researchers at the University of Houston (UH) have taken a significant step forward in unraveling the mechanisms of Pavlovian conditioning. Their work will help them understand how memories form and, ultimately, provide better treatments to improve memory in all ages.
Gregg Roman, an associate professor of biology and biochemistry at UH, and Shixing Zhang, his postdoctoral associate, describe their findings in a paper titled “Presynaptic Inhibition of Gamma Lobe Neurons Is Required for Olfactory Learning in Drosophila,” appearing Nov. 27 in Current Biology, a scientific bimonthly journal published by Cell Press.
“Memory is essential to our daily function and is also central to our sense of self,” Roman said. “To a large degree, we are the sum of our experiences. When memories can no longer be retrieved or we have difficulty in forming new memories, the effects are frequently tragic. In the future, our work will enable us to have a better understanding of how human memories form.”
Roman and Zhang set about to unravel some of these mysteries by studying the brains of fruit flies (Drosophila). Within the fly brain, Roman says, there are nerve cells that play a role in olfactory learning and memory. Olfactory learning, he says, is an example of classical conditioning first described by Pavlov in his experiment with dogs. In their study, the flies were trained to associate a weak electric shock with an odor. After training, the flies avoided that odor.
“We found that these particular nerve cells – the gamma lobe neurons of the mushroom bodies in the insect brain – are activated by odors. Training the flies to associate an odor with an electric shock changed how these cells responded to odors by developing a modification in gamma lobe neuron activity, known as a memory trace,” he said. “Interestingly, we found that training caused the gamma lobe neurons to be more weakly activated by odors that were not paired with an electric shock, while the odors paired with electric shock maintained a strong activation of these neurons. Thus, the gamma lobe neurons responded more strongly to the trained odor than to the untrained odor.”
The team also showed that a specific protein – the heterotrimeric G(o) protein – is naturally involved in inhibiting gamma lobe neurons. Roman says removing the activity of this protein only within the gamma lobe neurons resulted in a loss of the memory trace and, thus, poor learning. Therefore, inhibiting the release of neurotransmitters from these neurons through the actions of the G(o) protein is key to forming the memory trace and associative memories.
The significance of using fruit flies is that while their brain structure is much simpler with far fewer neurons, the mushroom body is analogous to the perirhinal cortex in humans, which serves the same function of sensory integration and learning. This simplicity allows scientists to gain insights into how memories are acquired, stored and retrieved.
“Drosophila represents the Goldilocks principle of neural research, with sufficient behavioral complexity, while maintaining a huge advantage in neural simplicity,” Roman said. “The complex behaviors allow us to examine many behavioral processes like learning, attention, aggression and addiction-like behaviors, while the simplicity allows us to dissect the crucial neural activities down to single cells. Additionally, Drosophila has the most powerful genetic toolkit available for behavioral experimentation. In using these tools, we are genetically identifying the molecules necessary to perform these behaviors and dissecting the logic of the neural circuits that allow for changes in behavior to occur.”
The pair says all their experience to date suggests the molecules and logic will translate to most animals, including humans, leading to a more complete understanding of how memories form in humans, both at the level of molecules and through the activity of neural circuits.
Neuron ‘claws’ in the brain enable flies to distinguish one scent from another
Think of the smell of an orange, a lemon, and a grapefruit. Each has strong acidic notes mixed with sweetness. And yet each fresh, bright scent is distinguishable from its relatives. These fruits smell similar because they share many chemical compounds. How, then does the brain tell them apart? How does the brain remember a complex and often overlapping chemical signature as a particular scent?
Researchers at Cold Spring Harbor Laboratory (CSHL) are using the fruit fly to discover how the brain integrates multiple signals to identify one unique smell. It’s work that has a broader implication for how flies – and ultimately, people – learn. In work published today in Nature Neuroscience, a team led by Associate Professor Glenn Turner describes how a group of neurons in the fruit fly brain recognize multiple individual chemicals in combination in order to define, or remember, a single scent.
The olfactory system of a fruit fly begins at the equivalent of our nose, where a series of neurons sense and respond to very specific chemicals. These neurons pass their signal on to a group of cells called projection neurons. Then the signal undergoes a transformation as it is passed to a body of neurons in the fly brain called Kenyon cells.
Kenyon cells have multiple, extremely large protrusions that grasp the projection neurons with a claw-like structure. Each Kenyon cell claw is wrapped tightly around only one projection neuron, meaning that it receives a signal from just one type of input. In addition to their unique structure, Kenyon cells are also remarkable for their selectivity. Because they’re selective, they aren’t often activated. Yet little is known about what in fact makes them decide to fire a signal.
Turner and colleague Eyal Gruntman, who is lead author on their new paper, used cutting-edge microscopy to explore the chemical response profile for multiple claws on one Kenyon cell. They found that each claw, even on a single Kenyon cell, responded to different odor molecules. Additional experiments using light to stimulate individual neurons (a technique called optogenetics) revealed that single Kenyon cells were only activated when several of their claws were simultaneously stimulated, explaining why they so rarely fire. Taken together, this work explains how individual Kenyon cells can integrate multiple signals in the brain to “remember” the particular chemical mixture as a single, distinct odor.
Turner will next try to determine “what controls which claws are connected, and how strong those connections are.” This will provide insight into how the brain learns to assign a specific mix of chemicals as defining a particular scent. But beyond simple odor detection, the research has more general implications for learning. For Turner, the question driving his work forward is: what in the brain changes when you learn something?
From football to flies: lessons about traumatic brain injury
Faced with news of suicides and brain damage in former professional football players, geneticist Barry Ganetzky bemoaned the lack of model systems for studying the insidious and often delayed consequences linked to head injuries.
Then he remembered an unexplored observation from nearly 40 years ago: a sharp strike to a vial of fruit flies left them temporarily stunned, only to recover a short time later. At the time he had marked it only as a curiosity.
Now a professor of genetics at UW–Madison, Ganetzky is turning his accidental discovery into a way to study traumatic brain injury (TBI). He and David Wassarman, a UW professor of cell and regenerative biology, report this week (Oct. 14) in the Proceedings of the National Academy of Sciences on the first glimpses of the genetic underpinnings of susceptibility to brain injuries and links to human TBI.
TBIs occur when a force on the body jostles the brain inside the head, causing it to strike the inside of the skull. More than 1.7 million TBIs occur each year in the United States, about one-third due to falls and the rest mainly caused by car crashes, workplace accidents, and sports injuries. TBIs are also a growing issue in combat veterans exposed to explosions.
In many cases, the immediate effects of TBI are temporary and may seem mild — confusion, dizziness or loss of coordination, headaches, vision problems. But over time, impacts may lead to neurodegeneration and related symptoms, including memory loss, cognitive problems, severe depression, or Alzheimer’s-like dementia. Together TBIs cost tens of billions of dollars annually in medical expenses and indirect costs such as lost productivity.
Though TBIs can be classified from “mild” to “severe” based on symptoms, there is a poor understanding of the underlying medical causes.
“Unlike many important medical problems — high blood pressure, cancer, diabetes, heart disease — where we know something about the biology, we know almost nothing about TBI,” Ganetzky says. “Why does a blow to the head cause epilepsy? Or how does it lead down the road to neurodegeneration? Nobody has answers to those questions — in part, because it’s really hard to study in humans.”
Enter the fruit fly. The fly brain is encased in a hard cuticle analogous to the skull, and the basic mechanisms affecting nervous system function are the same in flies and mammals. In the new study, Ganetzky and Wassarman describe a way to reproducibly inflict traumas that seem to mimic the injuries and symptoms of human TBI.
“Now we have a system where we can look at the variables that are the inputs into TBI and determine the relative contributions of each to the pathological outcomes. That’s the real power of the flies,” says Wassarman.
As with humans, few flies die from the immediate impact. Afterward, though, the treated flies show many of the same physical consequences as humans who sustain concussions or other TBIs, including temporary incapacitation, loss of coordination and activation of the innate immune response in the short term, followed by neurodegeneration and sometimes an early death.
The researchers, led by Rebeccah Katzenberger, senior research specialist in the UW Department of Cell and Regnerative Biology, also found that age seems to play an important role. Older flies are more susceptible than younger ones to the effects of the impact and, Wassarman says, many of the outcomes of TBI are very similar to normal aging processes.
With this model, the researchers say, they can now draw on the vast collection of genetic tools and techniques available for fruit flies to probe the underlying drivers of damage.
“What we really want is to understand the immediate and long term consequences in cellular and molecular terms,” says Ganetzky. “From that understanding we can proceed in a more directed way to diagnostics and therapeutics.”
One of the key things they have already identified is the crucial role genetics plays in determining the outcome of an injury, revealed by the high degree of variability seen among different strains of flies. This finding may explain why all potential TBI drugs to date have failed in clinical trials despite showing promise in individual rodent models.
As Wassarman explains, “The heart of the problem of solving traumatic brain injury is that we’re all different.”
They are continuing to develop the model through large-scale genetic analysis and have already found that different sets of genes correlate with susceptibility in flies of different ages. With their system, they can also examine the effects of repeated injuries.
Ganetzky sees tremendous potential for developing applications from the fly-based approach and the Wisconsin Alumni Research Foundation (WARF) has filed for patent protection on the discovery.
“These exciting findings that we can study traumatic brain injury — a disorder of growing concern for athletes, the military, and parents — in the elegantly simple model of fruit flies is sure to interest those researchers and companies looking to address this concern,” says Jennifer Gottwald, WARF licensing manager. “The use of this model can accelerate the work of the medical research community in finding treatments and therapies to help patients.”
(Source: news.wisc.edu)
Drowsy Drosophila shed light on sleep and hunger
Scientists discover key function in molecule that regulates sleep, metabolism and hunger
Why does hunger keep us awake and a full belly make us tired? Why do people with sleep disorders such as insomnia often binge eat late at night? What can sleep patterns tell us about obesity?
Sleep, hunger and metabolism are closely related, but scientists are still struggling to understand how they interact. Now, Brandeis University researchers have discovered a function in a molecule in fruit flies that may provide insight into the complicated relationship between sleep and food.
In the October issue of the journal Neuron, Brandeis scientists report that sNPF, a neuropeptide long known to regulate food intake and metabolism, is also an important component in regulating and promoting sleep. When researchers activated sNPF in fruit flies, the insects fell asleep almost immediately, awaking only long enough to eat before nodding off again. The flies were so sleepy that once they found a food source, they slept right on top of it for days — like falling asleep on a giant hamburger bun and waking up long enough to take a few nibbles before falling back to sleep.
When researchers returned sNPF functions to normal, the flies resumed their normal level of activity, leaving behind their couch potato ways.
The researchers, led by professor of biology Leslie Griffith, concluded that sNPF has an important regulatory function in sleep in addition to its previously known function coordinating behaviors such as eating and metabolism.
"This paper provides a nice bridge between feeding behavior and sleep behavior with just a single molecule," says Nathan Donelson, a post doctoral fellow in Griffith’s lab and one of the study’s lead authors.
Neurons use neuropeptides to communicate a range of brain functions including learning, metabolism, memory and social behaviors. In humans, Neuropeptide Y functions similarly to sNPF and has been studied as a possible drug target for obesity treatment.
But scientists don’t fully understand how regulating neuropeptide function at specific times and in specific cells affects sleeping and eating. By studying sNPF in fruit flies, scientists can learn which cells, neurotransmitters and genes are involved in eating and sleeping; what processes turn on and inhibit the behaviors, and how sleep cells are relevant to hunger drive.
"Our paper makes a significant step into tying all these things together," says Donelson, "and that is extremely important down the road to our understanding of human health."
(Source: eurekalert.org)
UI study shows fruit fly is ideal model to study hearing loss in people
If your attendance at too many rock concerts has impaired your hearing, listen up.
University of Iowa researchers say that the common fruit fly, Drosophila melanogaster, is an ideal model to study hearing loss in humans caused by loud noise. The reason: The molecular underpinnings to its hearing are roughly the same as with people.
As a result, scientists may choose to use the fruit fly to quicken the pace of research into the cause of noise-induced hearing loss and potential treatment for the condition, according to a paper published this week in the online Early Edition of the journal Proceedings of the National Academy of Sciences.
“As far as we know, this is the first time anyone has used an insect system as a model for NIHL (noise-induced hearing loss),” says Daniel Eberl, UI biology professor and corresponding author on the study.
Hearing loss caused by loud noise encountered in an occupational or recreational setting is an expensive and growing health problem, as young people use ear buds to listen to loud music and especially as the aging Baby Boomer generation enters retirement. Despite this trend, “the molecular and physiological models involved in the problem or the recovery are not fully understood,” Eberl notes.
Enter the fruit fly as an unlikely proxy for researchers to learn more about how loud noises can damage the human ear. Eberl and Kevin Christie, lead author on the paper and a post-doctoral researcher in biology, say they were motivated by the prospect of finding a model that may hasten the day when medical researchers can fully understand the factors involved in noise-induced hearing loss and how to alleviate the problem. The study arose from a pilot project conducted by UI undergraduate student Wes Smith, in Eberl’s lab.
“The fruit fly model is superior to other models in genetic flexibility, cost, and ease of testing,” Christie says.
The fly uses its antenna as its ear, which resonates in response to courtship songs generated by wing vibration. The researchers exposed a test group of flies to a loud, 120 decibel tone that lies in the center of a fruit fly’s range of sounds it can hear. This over-stimulated their auditory system, similar to exposure at a rock concert or to a jack hammer. Later, the flies’ hearing was tested by playing a series of song pulses at a naturalistic volume, and measuring the physiological response by inserting tiny electrodes into their antennae. The fruit flies receiving the loud tone were found to have their hearing impaired relative to the control group.
When the flies were tested again a week later, those exposed to noise had recovered normal hearing levels. In addition, when the structure of the flies’ ears was examined in detail, the researchers discovered that nerve cells of the noise-rattled flies showed signs that they had been exposed to stress, including altered shapes of the mitochondria, which are responsible for generating most of a cell’s energy supply. Flies with a mutation making them susceptible to stress not only showed more severe reductions in hearing ability and more prominent changes in mitochondria shape, they still had deficits in hearing 7 days later, when normal flies had recovered.
The effect on the molecular underpinnings of the fruit fly’s ear are the same as experienced by humans, making the tests generally applicable to people, the researchers note.
“We found that fruit flies exhibit acoustic trauma effects resembling those found in vertebrates, including inducing metabolic stress in sensory cells,” Eberl says. “Our report is the first to report noise trauma in Drosophila and is a foundation for studying molecular and genetic conditions resulting from NIHL.”
“We hope eventually to use the system to look at how genetic pathways change in response to NIHL. Also, we would like to learn how the modification of genetic pathways might reduce the effects of noise trauma,” Christie adds.
Administering Natural Substance Spermidin Stopped Dementia
Scientists from Freie Universität Berlin and the University of Graz Have Shown That Feeding Fruit Flies with Spermidin Suppresses Age-dependent Memory Impairment
Age-induced memory impairment can be suppressed by administration of the natural substance spermidin. This was found in a recent study conducted by Prof. Dr. Stephan Sigrist from Freie Universität Berlin and the Neurocure Cluster of Excellence and Prof. Dr. Frank Madeo from Karl-Franzens-Universität Graz. Both biologists, they were able to show that the endogenous substance spermidine triggers a cellular cleansing process, which is followed by an improvement in the memory performance of older fruit flies. At the molecular level, memory processes in animal organisms such as fruit flies and mice are similar to those in humans. The work by Sigrist and Madeo has potential for developing substances for treating age-related memory impairment. The study was first published in the online version of Nature Neuroscience.
Aggregated proteins are potential candidates for causing age-related dementia. With increasing age, the proteins accumulate in the brains of fruit flies, mice, and humans. In 2009 Madeo’s group in Graz already found that the spermidin molecule has an anti-aging effect by setting off autophagy, a cleaning process at the cellular level. Protein aggregates and other cellular waste are delivered to lysosomes, the digestive apparatus in cells, and degraded.
Feeding the fruit flies spermidin significantly reduced the amount of protein aggregates in their brains, and their memories improved to juvenile levels. This can be measured because flies can learn under classical Pavovian conditioning and adjust their behavior accordingly.
In humans, memory capacity decreases beginnning around the age of 50. This loss accelerates with increasing age. Due to increasing life expectancy, age-related memory impairment is expected to increase drastically. The spermidine concentration increases with age in flies as in humans. If it were possible to delay the onset of age-related dementia by giving individuals spermidin as a food supplement, it would be a great breakthrough for individuals and for society. Patient studies are the next step for Sigrist and Madeo.
(Source: fu-berlin.de)