Aging  

Researchers have discovered that melatonin supplements make bones stronger in elderly rats and therefore, potentially, in elderly humans too.

Faleh Tamimi, a professor in McGill’s School of Dentistry, is the leader of a research team that has just discovered that melatonin supplements make bones stronger in elderly rats and could, potentially, in elderly humans too. “Old rats are tedious to work with because they get sick a lot and that means they also cost a lot more. But if you’re interested in diseases like osteoporosis, they’re an essential part of the process.”

The study has been published in the journal, Rejevenation Research. 

"Until there is more research as well as clinical trials to determine how exactly the melatonin is working, we can’t recommend that people with osteoporosis go ahead and simply take melatonin supplements."

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The process of bone breakdown and buildup is affected by our circadian rhythms. The cells which break down our bones (known as osteoclasts) are more active at night, while those responsible for bone formation (osteoblasts) are more active during daylight hours.  “As we age, we sleep less well, which means that the osteoclasts are more active,” says Tamimi.  “This tends to speed up the process of bone breakdown.”

It is already well established that melatonin plays a role in regulating our body clocks and can potentially help us sleep better. So the researchers suspected that a melatonin supplement would help regulate the circadian rhythms of the elderly rats, thus reducing the activity of the osteoclasts and slowing down the process of bone breakdown. And that is exactly what they found.

Researchers at the University of Madrid, where the rats were housed, gave twenty 22-month-old male rats (the equivalent of 60 year-old humans) melatonin supplements diluted in water for 10 weeks (the equivalent of six years in human years). The femurs taken from the elderly rats which had received the melatonin supplements were then compared with those of a control group (which had not received the supplements) using a series of tests to measure bone density and strength.

The researchers found that there was a significant increase in both bone volume and density among the rats that had received melatonin supplements. As a result, it took much more force to break the bones of rats that had taken the melatonin supplements, a finding that suggests to the researchers that melatonin may prove a useful tool in combatting osteoporosis.

For Tamimi and his colleagues the next big question is whether melatonin is preventing or actually reversing the process of bone breakdown.  “Until there is more research as well as clinical trials to determine how exactly the melatonin is working, we can’t recommend that people with osteoporosis go ahead and simply take melatonin supplements,” says Tamimi. “I am applying for funding to pursue the research and we hope to have answers soon.”


SOURCE  McGill University

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 Biological Clock  

Researchers have discovered a new mechanism that governs how body clocks react to changes in the environment. The discovery could provide a solution for alleviating the detrimental effects of chronic shift work and jet-lag.

Researchers from The University of Manchester have discovered a new mechanism that governs how body clocks react to changes in the environment.

The discovery, which is being published in Current Biology, could provide a solution for alleviating the detrimental effects of chronic shift work and jet lag.

The team’s findings reveal that the enzyme casein kinase 1epsilon (CK1epsilon) controls how easily the body’s clockwork can be adjusted or reset by environmental cues such as light and temperature.

"It is now becoming clear that clock disruption is increasing the incidence and severity of diseases including obesity and diabetes."

Internal biological timers (circadian clocks) are found in almost every species on the planet. In mammals including humans, circadian clocks are found in most cells and tissues of the body, and orchestrate daily rhythms in our physiology, including our sleep/wake patterns and metabolism.

Dr David Bechtold, who led The University of Manchester’s research team, said: “At the heart of these clocks are a complex set of molecules whose interaction provides robust and precise 24 hour timing. Importantly, our clocks are kept in synchrony with the environment by being responsive to light and dark information.”

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The research identifies a new mechanism through which our clocks respond to these light inputs. During the study, mice lacking CK1epsilon, a component of the clock, were able to shift to a new light-dark environment (much like the experience in shift work or long-haul air travel) much faster than normal.

The research team went on to show that drugs that inhibit CK1epsilon were able to speed up shift responses of normal mice, and critically, that faster adaption to the new environment minimised metabolic disturbances caused by the time shift.

Dr Bechtold said: “We already know that modern society poses many challenges to our health and wellbeing - things that are viewed as commonplace, such as shift-work, sleep deprivation, and jet lag disrupt our body’s clocks. It is now becoming clear that clock disruption is increasing the incidence and severity of diseases including obesity and diabetes.

“We are not genetically pre-disposed to quickly adapt to shift-work or long-haul flights, and as so our bodies’ clocks are built to resist such rapid changes. Unfortunately, we must deal with these issues today, and there is very clear evidence that disruption of our body clocks has real and negative consequences for our health.”

He continues: “As this work progresses in clinical terms, we may be able to enhance the clock’s ability to deal with shift work, and importantly understand how maladaptation of the clock contributes to diseases such as diabetes and chronic inflammation.”


SOURCE  University of Manchester

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 Neuroscience  

Russell Foster shares three popular theories about why we sleep, busts some myths about how much sleep we need at different ages - and hints at some bold new uses of sleep as a predictor of mental health.

Russell Foster is a circadian neuroscientist: He studies the sleep cycles of the brain. And he asks: What do we know about sleep? Not a lot, it turns out, for something we do with one-third of our lives.

In this TEDx talk, Foster shares three popular theories about why we sleep, busts some myths about how much sleep we need at different ages -- and hints at some bold new uses of sleep as a predictor of mental health.

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Foster is Professor of Circadian Neuroscience and the Head of Department of Ophthalmology. He is also a Nicholas Kurti Senior Fellow at Brasenose College. Prior to this, Foster was at Imperial College where Foster was Chair of Molecular Neuroscience within the Faculty of Medicine. His research spans basic and applied circadian and photoreceptor biology.

For his discovery of non-rod, non-cone ocular photoreceptors he has been awarded the Honma prize (Japan), Cogan award (USA), and Zoological Society Scientific & Edride-Green Medals (UK). He is the co-author of Rhythms of Life: The Biological Clocks that Control the Daily Lives of Every Living Thing, a popular science book on circadian rhythms.

SOURCE  TEDx Talks

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 Neuroscience  

In a recent issue of Neuron, researchers report the discovery of a crucial part of the biological clock: the wiring that sets its accuracy to within a few minutes out of the 1440 minutes per day. This wiring uses the neurotransmitter, GABA, to connect the individual cells of the biological clock in a fast network that changes strength with time of day.

The World Health Organization lists shift work as a potential carcinogen, says Erik Herzog, PhD, Professor of Biology in Arts & Sciences at Washington University in St. Louis. And that’s just one example among many of the troubles we cause ourselves when we override the biological clocks in our brains and pay attention instead to the mechanical clocks on our wrists.

In a recent issue of Neuron, Herzog and his colleagues report the discovery of a crucial part of the biological clock: the wiring that sets its accuracy to within a few minutes out of the 1440 minutes per day. This wiring uses the neurotransmitter, GABA, to connect the individual cells of the biological clock in a fast network that changes strength with time of day.

Daily rhythms of sleep and metabolism are driven by a biological clock in the suprachiasmatic nucleus (SCN), a structure in the brain made up of 20,000 neurons, all of which can keep daily (circadian) time individually.

If the SCN is to be a robust, but sensitive, timing system, the neurons must synchronize precisely with one another and adjust their rhythms to those of the environment.

Herzog’s lab has discovered a push-pull system in the SCN that does both. In 2005 they reported that the neurons in the clock network communicate by means of a neuropeptide (VIP) that pushes them to synchronize with one another.

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As the researchers now report, these neurons also communicate with GABA that pulls on them weakly, so they are not too tightly coupled.

Together these two networks (VIP and GABA) ensure the clock runs as coordinated, precise timepiece but one that can still adjust its timing to synchronize with the environment.
“We think the neurotransmitter network is there to introduce enough jitter into the system to allow the neurons to resynchronize when environmental cues change, as they do with the seasons,” Herzog says.

But, he says, since this biological ‘reset button’ evolved long before mechanical clocks, artificial lights, and high-speed travel, it doesn’t introduce enough jitter to allow us to adjust quickly to the extreme time shifts of modern life, such as flying “backward” (east) through several time zones.

Understanding the push-pull system in the SCN has enormous implications for public health, bearing, as it does, on daylight saving times, shift work, school starting times, medical intern schedules, truck driver hours, and many other issues where the clock in the brain is pitted against the clock in the hand.

The problem is knowing if that increase was a coincidence or a consequence. The technique, called BSAC (Between Sample Analysis of Connectivity) reliably reveals functional connections by first describing the statistics of impossible connections. If the two neurons are in different dishes, they cannot communicate so the increased firing of neuron 2 must have been a coincidence.

By recording from lots of neurons in independent networks, BSAC defines the weakest possible connections that can be detected within a neural network. This could be useful in mapping connections between pairs of neurons or between brain regions.

The goal of the recent work in the Herzog lab has been to figure out how the clock cells are connected to each other. “It wasn’t clear, for example, if each neuron communicated with just a few of its neighbors or with all of them,” Herzog says.

In this network the connections are made by the neurotransmitter GABA (γ-amino-butyric acid). “We proved we had found a GABAergic network by applying drugs that block GABA receptors on the cells,” Herzog says. “All of the connections we had mapped between neurons dropped out.”

Remarkably, when the network drops out, the clock becomes more precise. So the GABAergic network destabilizes the clock; it jiggles it a little.

Herzog points out that the GABAergic network, is sparse, weak and fast (much faster than the VIP network, which relies on the slower action of a neuropeptide), as you might expect a jitter-generator to be.

“We think the GABAergic network is there to let our clocks adjust to environmental cues, such as gradual, seasonal changes in sunrise and sunset,” says Herzog.

It’s a bit like whacking an old television set that has lost vertical synch to get it to resynch with the broadcast signal.

But there isn’t enough jitter in the clock to allow it to make abrupt adjustments, such as the one-hour forward jump when Daylight Savings Time starts. That “spring forward” has been statistically shown to increase the likelihood of heart attacks and car accidents, Herzog says.

In any case, it is clear that if people repeatedly force the clock to reset, they throw off more than sleep. The biological clock regulates metabolism and cell division as well as sleep/wake cycles. So shift work, for example, is associated both with metabolic disorders, such as diabetes, and with the unregulated cell division that characterizes cancer.

Herzog points out that the neurons in the SCN are coupled oscillators, like these metronomes on a table that has enough give that each metronome’s motion affects the others’. Like the metronomes, the neurons keep time individually and because they are coupled by the VIP network, they synchronize their beats. Video by the Ikeguchi Laboratory, in the graduate school of science and engineering at Saitama University in Japan.

SOURCE  Washington University in St. Louis

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