Alcoholism may be caused by dynamical dopamine imbalance

Researchers from the Higher School of Economics, Ecole Normale Supérieure, Paris, Indiana University and the Russian Academy of Sciences Nizhny Novgorod Institute of Applied Physics have identified potential alcoholism mechanisms, associated with altered dopaminergic neuron response to complex dynamics of prefrontal cortex neurons affecting dopamine release.

Interacting neuronal populations in the cerebral cortex generate electrical impulses (called action potentials), that are characterized by specific spatial and temporal patterns of neural firing (or complex neural dynamics). These firing patterns depend on the intrinsic properties of individual neurons, on the neural network connectivity and the inputs to these circuits. Taken as a basis for this computational study is the experimental evidence for a specific population of prefrontal cortex neurons that connects via excitatory synapses to dopaminergic and inhibitory ventral tegmental area (VTA) neurons. Thus, the structure of neural firing in the prefrontal cortex can directly affect dopamine cell response and dopamine release.

Boris Gutkin leads the Theoretical Neuroscience Group at the HSE Centre for Cognition and Decision Making. One of the group’s research areas focuses on neurobiological processes leading to substance abuse and addiction — specifically, on detecting links between the neurobiological mechanisms of a drug’s action and observable behavioural reactions. In particular, the researchers use mathematical modelling to examine specific characteristics of dopaminergic neuron firing patterns and dynamics which can lead to addiction.

Dopamine, a neurotransmitter released by dopaminergic neurons in the brain, is a chemical which plays a key role in the internal brain reward system that drives learning of motivated behavior. By acting within the reward systems in the brain (e.g. the ventral tegmental area found deep in the mid-brain; the striatum, responsible for selecting correct actions and the prefrontal cortex that controls voluntary goals and behaviors), it signals either unexpected reward or anticipation of reward resulting from a particular action or event. Thus, dopamine provides positive reinforcement of behaviours that lead to these rewards, causing them to be repeated. Conversely, where a particular action fails to produce the expected positive effect or is followed by an unpleasant event, dopamine release decreases sharply, leading to frustration and an unwillingness to repeat the behaviour in question.

Many dopamine neurons produce these learning signals by emitting rapid bursts of spikes when the animal receives more reward than expected or pausing when there is less than expected. In order to govern the learning correctly, the number of bursts (and the dopamine released) must be proportional to the discrepancy between the received and the expected reward (for example if one expects to get 50 euros for his work, but gets 100; the dopamine activity should be proportional to 50; when one expects 50 but gets 500; the activity should signal a number proportional to 450). Hence the bigger the mismatch — the stronger the response. Yet another subgroup of dopamine neurons simply signals when stimuli are important for behaviour or not giving binary all or none responses. These binary signals then drive orienting or approach to the important behaviors. So the two dopamine cell populations have different response modes: analogue learning signal or all-or-none important alert.

Two Modes of neuron Activity

Recent research by Gutkin’s group conducted jointly with scientists from Indiana University (Alexey Kuznetsov, Mathematics and Christopher Lapish, Neuroscience) and the RAN Institute of Applied Physics (Denis Zakharov) suggests potential mechanisms of alcohol’s effect on dopaminergic neuronal activity. Their paper ‘Dopamine Neurons Change the Type of Excitability in Response to Stimuli’ published in PLOS features a computational model of dopamine (DA) neuron activity, describing its key properties and demonstrating that the DA neuron’s response mode can vary depending on the pattern of the synaptic input (including that from the prefrontal cortex).

When in the first mode, the amount of dopamine released by the DA neurons reflects the learning signal propotional to the difference between what an animal or human expects and what they actually receive as a result of a certain action. When in the second DA neuron mode, dopamine release serves as a reference binary signal indicating whether or not a certain event is important. Hence the results of the computational study imply that dopamine neurons may not be two distinct populations, but are capable to move flexibly from one response mode to another depending on the nature of the signals they receive.

In a related study, ‘Contribution of synchronized GABAergic neurons to dopaminergic neuron firing and bursting’, published in the Journal of Neurophysiology the same group suggests that in addition to direct links between DA and prefrontal cortex neurons, indirect neural inputs from the prefrontal cortex via inhibitory (GABAergic) VTA neurons should be considered. In particular, the researchers found that signals from the prefrontal cortex can cause GABAergic neurons to synchronise, producing a strong inhibitory effect on DA neurons. The study found that in some cases, such inhibitory effects can lead to paradoxical results: instead of suppressing DA neuron firing and thus decreasing dopamine release, they can multiply DA firing frequency leading to higher dopamine release and positive reinforcement.

What It Means for Our Understanding of Alcoholism

Experimental evidence suggests that alcohol is capable of modifying DA neuron firing patterns, both indirectly via prefrontal cortex and inhibitory VTA neurons, and directly by acting on DA neurons per se. Based on Gutkin and his collaborators findings, one can hypothesise what mechanisms may be involved.

The VTA has about 20,000 DA neurons, in someone who is not alcoholic, some of these serve to signal that a certain stimulus has importance, while the rest transmit the error signal. A certain balance between the two types of signals is essential for good judgment and proper behaviour. Alcohol disrupts the balance by changing both the pattern of neural activity in the prefrontal cortex and DA neuron properties. This change may bias more neurons to signal importance as opposed to the error. So, under alcohol influence, any stimulus associated with alcohol is treated by DA neurons as having behavioural and motivational importance, regardless of whether or not it matches the anticipated outcome, while in the absence of alcohol, neural firing would normally be consistent with the expected and received reinforcements.

This effect may be the reason why alcoholics may eventually develop a narrower than normal range of behavioural responses, dooming them to seek to use alcohol. In doing so, they are either unaware of potential consequences of their actions or, even if they can anticipate such consequences, this awareness has little or no effect on their behaviour. According to surveys, most alcoholics understand that they may lose their home and family and even die from binge drinking, but this rarely stops them. To properly assess the consequences of drinking, their prefrontal cortex needs to integrate and learn to properly represent the negative expectations from this behaviour, supported by reinforcement learning signals from DA neurons. This may not happen, however, because alcohol (like other mood-altering substances) can affect both the neural activity in the addict’s prefrontal cortex and their DA neurons directly, blocking the learning.

Finding a way to balance out the dopamine function in the addicted brain and to elicit adequate neural responses to environmental stimuli even under the influence could offer hope to people with substance abuse problems.

 

Incidence of dementia in primary care increased in the Netherlands over 23 years

The incidence of registered dementia cases has increased slightly over a 23-year period (1992 to 2014) in the Netherlands, according to a study published by Emma van Bussel and colleagues from the Academic Medical Center Amsterdam, The Netherlands, in PLOS Medicine‘s Special Issue on Dementia.

The researchers collected data on dementia diagnoses for persons aged 60 years and over from general practitioner networks for the years 1992 to 2014, including data on more than 800,000 older people and 23,186 incident dementia cases. They estimate that the annual growth in dementia incidence rate is 2.1% (95% CI 0.5% to 3.8%), with incidence rates 1.08 (95% CI 1.04 to 1.13) times higher for women compared to men. The authors say that increased awareness of dementia by patients and doctors in more recent years may have influenced dementia diagnosis by general practitioners in electronic health records, and needs to be taken into account when interpreting the data.

In a linked Perspective, Eric Larson discusses the findings in light of previous cohort studies that have reported a recent decline in dementia incidence rates and highlights that studies on the incidence and prevalence of dementia can provide insights into possible strategies to control dementia.

He says: “We must plan for increasing numbers of predominantly older people with dementia in the decades to come including addressing the growing need for long-term care in the context of a significant decline in the availability of family caregivers.”

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Caffeine boosts enzyme that could protect against dementia

A study by Indiana University researchers has identified 24 compounds — including caffeine — with the potential to boost an enzyme in the brain shown to protect against dementia.

The protective effect of the enzyme, called NMNAT2, was discovered last year through research conducted at IU Bloomington. The new study appears today in the journal Scientific Reports.

“This work could help advance efforts to develop drugs that increase levels of this enzyme in the brain, creating a chemical ‘blockade’ against the debilitating effects of neurodegenerative disorders,” said Hui-Chen Lu, who led the study. Lu is a Gill Professor in the Linda and Jack Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, a part of the IU Bloomington College of Arts and Sciences.

Previously, Lu and colleagues found that NMNAT2 plays two roles in the brain: a protective function to guard neurons from stress and a “chaperone function” to combat misfolded proteins called tau, which accumulate in the brain as “plaques” due to aging. The study was the first to reveal the “chaperone function” in the enzyme.

Misfolded proteins have been linked to neurodegenerative disorders such as Alzheimer’s, Parkinson’s and Huntington’s diseases, as well as amyotrophic lateral sclerosis, also known as ALS or Lou Gehrig’s disease. Alzheimer’s disease, the most common form of these disorders, affects over 5.4 million Americans, with numbers expected to rise as the population ages.

To identify substances with the potential to affect the production of the NMNAT2 enzyme in the brain, Lu’s team screened over 1,280 compounds, including existing drugs, using a method developed in her lab. A total of 24 compounds were identified as having potential to increase the production of NMNAT2 in the brain.

One of the substances shown to increase production of the enzyme was caffeine, which also has been shown to improve memory function in mice genetically modified to produce high levels of misfolded tau proteins.

Lu’s earlier research found that mice altered to produce misfolded tau also produced lower levels of NMNAT2.

To confirm the effect of caffeine, IU researchers administered caffeine to mice modified to produce lower levels of NMNAT2. As a result, the mice began to produce the same levels of the enzyme as normal mice.

Another compound found to strongly boost NMNAT2 production in the brain was rolipram, an “orphaned drug” whose development as an antidepressant was discontinued in the mid-1990s. The compound remains of interest to brain researchers due to several other studies also showing evidence it could reduce the impact of tangled proteins in the brain.

Other compounds shown by the study to increase the production of NMNAT2 in the brain — although not as strongly as caffeine or rolipram — were ziprasidone, cantharidin, wortmannin and retinoic acid. The effect of retinoic acid could be significant since the compound derives from vitamin A, Lu said.

An additional 13 compounds were identified as having potential to lower the production of NMNAT2. Lu said these compounds are also important because understanding their role in the body could lead to new insights into how they may contribute to dementia.

“Increasing our knowledge about the pathways in the brain that appear to naturally cause the decline of this necessary protein is equally as important as identifying compounds that could play a role in future treatment of these debilitating mental disorders,” she said.

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Blueberry concentrate improves brain function in older people

Drinking concentrated blueberry juice improves brain function in older people, according to research by the University of Exeter.

In the study, healthy people aged 65-77 who drank concentrated blueberry juice every day showed improvements in cognitive function, blood flow to the brain and activation of the brain while carrying out cognitive tests.

There was also evidence suggesting improvement in working memory.

Blueberries are rich in flavonoids, which possess antioxidant and anti-inflammatory properties.

Dr Joanna Bowtell, head of Sport and Health Sciences at the University of Exeter, said: “Our cognitive function tends to decline as we get older, but previous research has shown that cognitive function is better preserved in healthy older adults with a diet rich in plant-based foods.

“In this study we have shown that with just 12 weeks of consuming 30ml of concentrated blueberry juice every day, brain blood flow, brain activation and some aspects of working memory were improved in this group of healthy older adults.”

Of the 26 healthy adults in the study, 12 were given concentrated blueberry juice — providing the equivalent of 230g of blueberries — once a day, while 14 received a placebo.

Before and after the 12-week period, participants took a range of cognitive tests while an MRI scanner monitored their brain function and resting brain blood flow was measured.

Compared to the placebo group, those who took the blueberry supplement showed significant increases in brain activity in brain areas related to the tests.

The study excluded anyone who said they consumed more than five portions of fruit and vegetables per day, and all participants were told to stick to their normal diet throughout.

Previous research has shown that risk of dementia is reduced by higher fruit and vegetable intake, and cognitive function is better preserved in healthy older adults with a diet rich in plant-based foods.

Flavonoids, which are abundant in plants, are likely to be an important component in causing these effects.

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New study sheds light on perceptions of e-cigs

Daily users of e-cigarettes see them as about as satisfying or even more satisfying, and less harmful, than cigarettes, according to the results of a small study from the University at Buffalo.

The study of 105 U.S. Army Reserve and National Guard soldiers and their partners found that those study participants who vape daily reported e-cigarettes as “at least as satisfying” as cigarettes, and that 58 percent said vaping was “much more” satisfying.

Researchers also reported that the perception of danger from e-cigarettes decreased as frequency of use increased. The paper was published online first in the journal Preventive Medicine Reports.

“The results argue that satisfaction, perceived harm or danger and product type seem to all work together to promote use or avoidance,” said Lynn Kozlowski, the paper’s lead author and a professor of community health and health behavior in UB’s School of Public Health and Health Professions.

“The mistaken belief that e-cigarettes are more harmful than cigarettes can influence some smokers to not use e-cigs. If the type of product they use is less satisfying, this also can influence likelihood of use,” Kozlowski, PhD, added.

Kozlowski’s co-authors, both from UB, are Gregory Homish, PhD, associate professor and associate chair of community health and health behavior, and D. Lynn Homish, project director for Operation: SAFETY (Soldiers and Families Excelling Through the Years), a longitudinal research study examining the health and well-being of more than 400 U.S. Army Reserve and National Guard soldiers and their partners.

A subset of the Operation: SAFETY sample size was used for this study, which was funded by the National Institute of Drug Abuse.

In their paper, the researchers note that the findings regarding e-cigarette satisfaction are important because of policies that have been implemented based on the belief that e-cigarettes are fundamentally lacking in satisfaction compared to cigarettes.

The concern that vaping acts as a “gateway” to cigarettes is more credible if vaping is less satisfying than smoking. For vaping products that are much more satisfying than cigarettes and also perceived as less dangerous than cigarettes, it is less likely that users would want to switch to cigarettes in the future, the researchers point out.

“Many people believe that vaping could not be as satisfying as cigarettes, and this lack of satisfaction could encourage switching to the more satisfying product. But our findings indicate that that the non-cigalike vaping products can be very satisfying,” Kozlowski said.

The first-generation vaping products that came to market are often called ‘cigalikes’ — they’re electronic cigarettes designed to look and feel like traditional cigarettes. “There is growing evidence that the cigalike products are less effective at delivering nicotine than the newer types of vaping products,” Kozlowski said.

The newer devices, which are generally larger, are sometimes referred to as non-cigalikes.

While the sample size is small, the study’s results do show something important about the role e-cigarettes can play in harm reduction, says Kozlowski.

“Those who try to exaggerate fears of vaping products should consider their role in keeping smokers smoking,” he said. “Telling people only that no product is ‘safe’ is an irresponsible message.”

Instead, Kozlowski said, public health experts need to continue stressing the well-documented dangers of cigarettes and what is likely to be true about differential risks.

“Those smokers who have tried only cig-alike products should know that they may be able to find a more satisfying substitute for smoking in other vaping products,” he adds. “The focus should be giving up smoking completely first. After that, we would also encourage giving up vaping, provided it doesn’t cause a return to smoking.”

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Painkillers without dangerous side effects

Researchers from Charité — Universitätsmedizin Berlin have discovered a new way of developing painkillers. The team of researchers used computational simulation to analyze interactions at opioid receptors — the cell’s docking sites for painkillers. When used in an animal model, their prototype of a morphine-like molecule was able to produce substantial pain relief in inflamed tissues. However, healthy tissues remained unaffected, suggesting that the severe side effects currently associated with these types of painkillers might be avoided. This research has been published in the current issue of the journal Science.

Opioids are a class of strong pain killers. They are mainly used to treat pain associated with tissue damage and inflammation, such as that caused by surgery, nerve damage, arthritis or cancer. Common side effects associated with their use include drowsiness, nausea, constipation and dependency and, in some cases, respiratory arrest. “By analyzing drug-opioid receptor interactions in damaged tissues, as opposed to healthy tissues, we were hoping to provide useful information for the design of new painkillers without harmful side effects,” explains Prof. Dr. Christoph Stein, Head of the Department of Anesthesiology and Surgical Critical Care Medicine on Campus Benjamin Franklin. In cooperation with PD Dr. Marcus Weber from the Zuse Institute Berlin, and with the help of innovative computational simulations, the researchers were able to analyze morphine-like molecules and their interactions with opioid receptors. They were able to successfully identify a new mechanism of action, which is capable of producing pain relief only in the desired target tissues — those affected by inflammation.

Treating postoperative and chronic inflammatory pain should now be possible without causing side effects. Doing so would substantially improve patient quality of life. The study’s first authors, Dr. Viola Spahn and Dr. Giovanna Del Vecchio, explain: “In contrast to conventional opioids, our NFEPP-prototype appears to only bind to, and activate, opioid receptors in an acidic environment. This means it produces pain relief only in injured tissues, and without causing respiratory depression, drowsiness, the risk of dependency, or constipation.” After designing and synthesizing the drug prototype, the researchers subjected it to experimental testing. Using computer modeling, the researchers simulated an increased concentration of protons, thereby mimicking the acidic conditions found in inflamed tissues. “We were able to show that the protonation of drugs is a key requirement for the activation of opioid receptors,” conclude the authors. Their findings, which may also apply to other types of pain, may even find application in other areas of receptor research. Thereby, the benefits of improved drug efficacy and tolerability are not limited to painkillers, but may include other drugs as well.

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Social rejection by those closest to you can lead to subsequent drinking

The need to belong and experience social connections is a fundamental human characteristic. Prior research has shown that social rejection is linked to increases in negative emotions, distress, and hostility. This study examined the impact of social rejection on alcohol use, and whether the impact differed when the social rejection was by close others, such as friends, spouses or family members, or by strangers or acquaintances.

Researchers gathered data from 77 community participants (41 women, 36 men) who used their smartphones to record their social interactions and alcohol use for 14 consecutive days. The analysis examined associations between rejection experiences and daily alcohol use.

Findings indicated that the type of relationship may be a key factor in whether or not social rejection leads to drinking. More specifically, on days characterized by rejection by close others, the likelihood of drinking significantly increased. In contrast, on days characterized by rejection by acquaintances, there was no increase in the likelihood of drinking. This finding contrasts with laboratory studies of rejection that emphasize rejection and ostracism by strangers rather than known others.


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Journal Reference:

  1. Holly B. Laws, Nicole E. Ellerbeck, Alyne S. Rodrigues, Jessica A. Simmons, Emily B. Ansell. Social Rejection and Alcohol Use in Daily Life. Alcoholism: Clinical and Experimental Research, 2017; DOI: 10.1111/acer.13347

Cite This Page:

Research Society on Alcoholism. “Social rejection by those closest to you can lead to subsequent drinking.” ScienceDaily. ScienceDaily, 3 March 2017. .

Research Society on Alcoholism. (2017, March 3). Social rejection by those closest to you can lead to subsequent drinking. ScienceDaily. Retrieved March 3, 2017 from www.sciencedaily.com/releases/2017/03/170303081232.htm

Research Society on Alcoholism. “Social rejection by those closest to you can lead to subsequent drinking.” ScienceDaily. www.sciencedaily.com/releases/2017/03/170303081232.htm (accessed March 3, 2017).

Studies show that the cerebellum is crucial to understanding vulnerability to drug addiction

An international research team led by the Universitat Jaume I (UJI) has shown that the cerebellum, contrary to what was thought, fulfils functions that go beyond the motor sphere and can be co-responsible for the brain alterations associated with addictive consumption of drugs. The findings, which are shown in two recent reviews published in Neuroscience & Biobehavioral Reviews and Journal of Neuroscience — with an image taken at the UJI laboratories — , would represent a step forward towards the design of new therapies for the future.

These studies are based on a series of works published over the last two years by the research group Addiction and Neuroplasticity at the Universitat Jaume I, directed by the lecturer of the Area of Psychobiology at ​​the UJI, which has had the collaboration of researchers from European, Mexican and North American universities. The most relevant, according to Miquel, is that the studies show that changes in the cerebellum “only occur in those subjects who appear to be especially vulnerable to the effect of drugs.” For a long time, “we have verified that the cerebellum responds in a very potent way to the effect of cocaine, to the point of changing the mechanisms of plasticity,” states Miquel, who is also coordinator of the master’s degree in Research in Brain and Behaviour.

Consequently, the cerebellum is a region of the brain relevant to understanding and designing future treatments for drug addiction. “There is progress in describing the neuronal circuits affected by drug addiction, a chronic brain disorder that is difficult to treat because it affects the basic processes of acquiring and storing the information whose description is still incomplete,” explains the teacher, who acknowledges that, in this way, “the path to new therapies will be accelerated.”

Addiction involves alterations in the neuronal mechanisms of plasticity that allow the brain to store information, regenerate itself and recover from possible disorders or injuries. In an addicted person, the brain’s mechanisms of learning and memory that allow you to make decisions and carry out acts of will are sick. Addictive drugs force the brain to store harmful data about where, when and how to consume the substance. In fact, the drug is the predominant information in the brains of people affected by addiction.

The Effects of Cocaine

On this occasion, the reviewed investigations address the function of the cerebellum in these storage processes involved in the addictive disorder. Specifically, “experimental work shows that these effects of cocaine on cerebellar function only occur in those individuals dominated by stimuli that predict drug availability and suggest that the cerebellum may be crucial to understanding mechanisms of vulnerability to addiction,” explains Marta Miquel.

Science has corroborated that certain regions of the brain, such as the prefrontal cortex, amygdala, hippocampus, and basal ganglia, may be relevant for addiction. However, the cerebellum had traditionally been excluded from this circuit because it was considered a structure exclusively dedicated to motor control, especially motor coordination. “Today we know that this is a very partial view on the complexity of the cerebellum, and a growing volume of data suggests its involvement in many of the brain functions affected in addicted subjects,” refers Marta Miquel. “The cerebellum comprises 80% of all neurons in the brain; it contains 60 billion neurons packaged in only 10% of the brain mass and is a fundamental structure in the consolidation and automation of learned behavioural repertoires,” concludes the lecturer.

In addition to the UJI team, scientists from the University of Kentucky (USA), University of Turin (Italy), Universidad Veracruzana (Mexico), Washington State University (USA), University of Cambridge, University of Leeds (United Kingdom), McLean Hospital Translational Neuroscience Laboratory and Mailman Research Center (USA) also participate in the research works. After presenting the papers at the last congress of the International Society for Neuroscience (San Diego, USA), the work will be discussed soon at the Albert Einstein Institute in New York.

The priority line of the research group Addiction and Neuroplasticity from the Universitat Jaume I, directed by the lecturer Marta Miquel, is the brain’s function in drug addiction.

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Alzheimer’s may be linked to defective brain cells spreading disease

Rutgers scientists say neurodegenerative diseases like Alzheimer’s and Parkinson’s may be linked to defective brain cells disposing toxic proteins that make neighboring cells sick.

In a study published in Nature, Monica Driscoll, distinguished professor of molecular biology and biochemistry, School of Arts and Sciences, and her team, found that while healthy neurons should be able to sort out and rid brain cells of toxic proteins and damaged cell structures without causing problems, laboratory findings indicate that it does not always occur.

These findings, Driscoll said, could have major implications for neurological disease in humans and possibly be the way that disease can spread in the brain.

“Normally the process of throwing out this trash would be a good thing,” said Driscoll. “But we think with neurodegenerative diseases like Alzheimer’s and Parkinson’s there might be a mismanagement of this very important process that is supposed to protect neurons but, instead, is doing harm to neighbor cells.”

Driscoll said scientists have understood how the process of eliminating toxic cellular substances works internally within the cell, comparing it to a garbage disposal getting rid of waste, but they did not know how cells released the garbage externally.

“What we found out could be compared to a person collecting trash and putting it outside for garbage day,” said Driscoll. “They actively select and sort the trash from the good stuff, but if it’s not picked up, the garbage can cause real problems.”

Working with the transparent roundworm, known as the C. elegans, which are similar in molecular form, function and genetics to those of humans, Driscoll and her team discovered that the worms — which have a lifespan of about three weeks — had an external garbage removal mechanism and were disposing these toxic proteins outside the cell as well.

Ilija Melentijevic, a graduate student in Driscoll’s laboratory and the lead author of the study, realized what was occurring when he observed a small cloud-like, bright blob forming outside of the cell in some of the worms. Over two years, he counted and monitored their production and degradation in single still images until finally he caught one in mid-formation.

“They were very dynamic,” said Melentijevic, an undergraduate student at the time who spent three nights in the lab taking photos of the process viewed through a microscope every 15 minutes. “You couldn’t see them often, and when they did occur, they were gone the next day.”

Research using roundworms has provided scientists with important information on aging, which would be difficult to conduct in people and other organisms that have long life spans.

In the newly published study, the Rutgers team found that roundworms engineered to produce human disease proteins associated with Huntington’s disease and Alzheimer’s, threw out more trash consisting of these neurodegenerative toxic materials. While neighboring cells degraded some of the material, more distant cells scavenged other portions of the diseased proteins.

“These finding are significant,” said Driscoll. The work in the little worm may open the door to much needed approaches to addressing neurodegeneration and diseases like Alzheimer’s and Parkinson’s.”

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