As per a latest research, slow walking might be associated with a major deficit in cognitive and physical health. From a longitudinal study of more than 900 New Zealanders which started in the 1970s,it has been found that people in 40s walking with slow gait are more likely to exhibit signs of increased biological ageing along with reduced brain integrity. The findings appear in the JAMA Network Open.
Line J.H. Rasmussen, biological researcher from Duke University said that it is indeed striking to observe this people with age of 45 years, not geriatric patients normally associated with such conditions. Rasmussen and his team studied participants from Dunedin Study, a very long longitudinal health study which was started almost fifty years ago having a cohort of more than 1000 three year olds. Assessing the health of the remaining 904 participants at age of 45, researchers found that the speed of walking at mid-life offered a way of identifying ageing processes extending all the way to childhood.
Terrie E. Moffitt, psychologist and neuroscientist at Duke said that the study assessed the time from preschool life to mid-life and found that slow walk is an indication of a problem decades before the actual old age. 45 year old participants in the study had their walking speed checked on several measures of daily physical functions. Signs of accelerated ageing were also assessed which included 19 different biomarkers from blood pressure to dental health along with brain scans by MRI. Past data were also considered such as neurocognitive abilities of participants of their childhood.
The results revealed that reduced walking speed in mid-40s is associated with deteriorated physical functioning and accelerated ageing. This is indicated by increased deterioration of several organ systems along with a different visual analysis of the ages of participants which were conducted by a panel. Authors also explain in the paper that gait speed was also related to neurocognitive functioning in childhood besides concurrent neurocognitive functioning. Brain scans were not conducted when the study started, however on the basis of current tests, it was shown that slow walkers on average had decreased brain volume and cortical thickness.
There are certain limitations in this study which includes lack of gait speed measurements in earlier tests with the cohort and lack of previous brain imaging data. However the scientists say that there are many things to be understood in the examination of the link between neurocognitive functioning at childhood and gait speed at midlife in the future research.
Stephanie Studenski, geriatric medicine researcher at the University of Pittsburgh said that bad results of cognitive testing in children of age three years should not be always connected to lifelong problems. Rather contributing factors to this poor performance and resultant coping up strategies should be considered.
From this decades old study, we can also identify the positive social influence factors that boost biological longevity along with neurocognitive functioning. The human brain is quite dynamic and it is reorganising itself constantly according to experience and exposure.
Hence the brain health which is reflected in the brain structure, gait speed and cognition might not be the first cause but consequence of insults and opportunities on a lifelong basis.
Researchers from Japan have kept small portions of mouse brain tissue alive and viable for a period of 25 days, isolating in a culture. This has highly increased the timeline in which the isolated brain tissue can keep the functions intact extending days to weeks. This can affect the research in therapeutic drugs in a positive way. The findings have been published in the Analytical Sciences journal.
The key to success was a new technique that combines a special kind of membrane with an improved microfluidic device. Microfluidic devices use small channels for delivery of fluid into tissues and are better than the normal culture dishes specially for ex vivotissue experiments. They can also be customized highly and mimic certain kinds of cell behaviors. They also require small volume samples thus making it easy to study the cell interactions.
However, only a few days is not sufficient to understand how body systems react to various things. The main problem is to keep a balance. Tissues dry quickly so the system has to be kept moist along with nutrients in a wet culture medium. Too much moisture prevents cells to exchange gases which the tissue needs thus drowning it finally. This problem had to be tackled by the researchers.
This device has a semi-permeable microfluidic channel that is surrounded by an artificial membrane and solid walls. These are made from polydimethylsiloxane, a polymer mainly used in microfluidic devices. The tissue does not sit in the bath consisting of the culture medium but instead, the fluid circulates through the channel, passing by the membrane to keep the tissues most while still maintaining the exchange of gases between cells.
Nobutoshi Ota, a biochemist at RIKEN Center for Biosystems Dynamics Research said that the medium flow was difficult to be controlled as the microchannel between the porous membrane and PDMS walls were not normal. The team got success after repeated trials and modifications to the membrane while adjusting the flow rates of the inlet and outlet.
A small part of the brain named suprachiasmatic nucleus(SCN) was used which is responsible for keeping the circadian and biological rhythms intact in mammals. Neuronal cells in SCN exchange information by keeping the motion of peptides and molecules between cells intact. This is ideal for studying cell interactions.
The mice from where the SCNs were harvested had been edited genetically such that the circadian rhythm in the brain was connected to the production of a fluorescent protein indicating if everything was working properly.
The fluorescence was active for 25 days compared to that of a normal culture dish where after 10 hours the activity control reduced by 6 percent. The experiment lasted for only 25 days since it was the cutoff time for this experiment. It could have lasted well beyond 100 days.
Researchers believe that this can also be used for remaining organ tissues with the possibility for human organs that are grown in the laboratory. This will improve the research in organogenesis by culturing and observation which is needed for the growth of organs and tissue.
September 29, 2019(updated September 29, 2019) Published by Kshitij Kumar
As per new research, a combination of stress and anxiety might physically change the makeup of the mitochondrial cells. In our lifetime, we often deal with events that leave a lasting impression on our minds. Major incidents such as losing a loved one, war, divorce can lead to anxiety disorders along with panic attacks. Anxiety disorder is different from normal worrying since it is prolonged and does not reduce with time. It can be bad for our emotional and physical health since it interferes with the normal daily activities making them difficult to perform.
According to the National Institute of Mental Health, anxiety disorders are impacted by a combination of our genes and the environment resulting in an overall stressful life. It has been observed that not all people facing traumatic events develop anxiety disorder raising the question of what makes some persons respond differently than others.
To find the answer, scientists studied mice that had displayed symptoms of depression and anxiety such as staying alone after facing highly stressful situations. Changes in the genetic activity were then tracked along with the production of protein in the area of the brain which deals with stress and anxiety. These areas are thehippocampus, prefrontal cortex, nucleus accumbens, and amygdala. The research team used the “cross-species multi-omics” technique for analyzing the genes and proteins that are associated with mitochondrial cells. They found many changes in the mitochondria of the mice’s brain cells who were exposed to stress as compared to those who were not. After that blood samples of the patients who had panic disorder were tested and scientists detected similar mitochondrial changes in them.
The researchers mentioned in PLOS Genetics that the studies revealed a regular convergence of differentially expressed pathways related to mitochondria in blood samples of patients dealing with a panic disorder after a panic attack. This method of cellular energy metabolism might be a way in which animals deal with stress.
Mitochondria, also known as thepowerhouse of cells turn the food consumed into 90 percent of the chemical energy needed for the functioning of the body along with destroying the rogue cells. Dealing with a high amount of stress can affect how the mitochondria function leading to complicated health symptoms.
Iiris Hovatta, University of Helsinki said that right now there is very little information on the effects of chronic stress on cellular energy metabolism. So these underlying mechanisms might be essential to the prevention of diseases related to stress. Genetic studies of the persons suffering from anxiety might lead to informed treatment which is currently limited to psychotherapy and medicines.
September 10, 2019(updated September 10, 2019) Published by Kalpit Veerwal
Scientists for the first time have been able to identify the specific gene regions which have an influence on being left-handed. They have also found connections to differences in the structure of the brain in those having these variations.
It has been established before that being left or right-handed has an approximate dependence of 25 percent on the genetic code at birth. However, until now, researchers have not been able to locate the specific areas of the genome that are responsible.
The latest study involved nearly 400,000 individual records in a national database of the United Kingdom. Four genetic regions were found that were associated with handedness out of which three were linked to the proteins in the development and structure of the brain. These proteins are related to the cytoskeleton which is responsible for the construction and functionality of the cells. The study appears in the Brain Journal.
Brain scans were performed on 10,000 participants through which researchers were able to link the variations in the genetic code with white matter tracts between the language-processing regions. The cytoskeleton of the brain is present in the white matter tracts. Akira Wiberg, physician said that the large datasets from the UK Biobank helped in a deep understanding of the processes responsible for left-handedness. The language areas in the left and right sides of the brain coordinate with each other in a coordinated manner for participants with left-handedness. This might translate to left-handers having better language and verbal skills.
Human beings have an imbalance between the left-handed and right-handed individuals which is a ratio of 1:9. Cytoskeletal differences like a coil of a snail’s shell can be highly influenced by genetics. Hence scientists think the indications of the development of handedness might be initiated in the mother’s womb.
We are still at an early stage of the research to say conclusively that handedness and genes are related however this research has provided significant associations between the two instances. Scientists are now starting to understand how a dominant hand is influenced by genetic coding. This also helps in preventing any misconceptions that left-handedness is a sign of being unlucky or that being a right-handed individual is somehow superior.
Dominic Furniss, a plastic surgeon researching in molecular genetics said that through this study it has been demonstrated that left-handedness is a result of the brain’s developmental biology which is also influenced by the complex genetic interplay.
Much of the research on the underlying causes of Alzheimer’s disease focuses on amyloid beta (Aß), a protein that accumulates in the brain as the disease progresses. Excess Aß proteins form clumps or “plaques” that disrupt communication between brain cells and trigger inflammation, eventually leading to widespread loss of neurons and brain tissue.
Aß plaques will continue to be a major focus for Alzheimer’s researchers. However, innovative research by neuroscientists at the University of Chicago looks at another process that plays an underappreciated role in the progression of the disease.
In a new study published in the Journal of Neuroscience, Prof. Sangram Sisodia, a leading expert on the biology of Alzheimer’s disease, and his colleagues show how in genetic forms of Alzheimer’s, a process called neurogenesis—the creation of new brain cells—can be disrupted by the brain’s own immune cells.
Some types of early onset, hereditary Alzheimer’s are caused by mutations in two genes called presenilin 1 (PS1) and presenilin 2 (PS2). Previous research has shown that when healthy mice are placed into an “enriched” environment where they can exercise, play and interact, they have a huge increase in new brain cells being created in the hippocampus—the part of the brain that is important for memory. But when mice carrying mutations to PS1 and PS2 are placed in an enriched environment, they don’t show the same increase in new brain cells. They also start to show signs of anxiety, a symptom often reported by people with early onset Alzheimer’s.
This led Sisodia to think that something besides genetics had a role to play. He suspected that the process of neurogenesis in mice both with and without Alzheimer’s mutations also could be influenced by other cells that interact with the newly forming brain cells.
The researchers focused on microglia, a kind of immune cell in the brain that usually repairs synapses, destroys dying cells and clears out excess Aß proteins. When the researchers gave the mice a drug that causes microglial cells to die, neurogenesis returned to normal. The mice with presenilin mutations were then placed into an enriched environment and they were fine; they didn’t show any memory deficits or signs of anxiety, and they were creating the normal, expected number of new neurons.
“It’s the most astounding result to me,” said Sisodia, the Thomas Reynolds Sr. Family Professor of Neurosciences at UChicago. “Once you wipe out the microglia, all these deficits that you see in these mice with the mutations are completely restored. You get rid of one cell type, and everything is back to normal.”
Sisodia thinks the microglia could be overplaying their immune system role in this case. Alzheimer’s disease normally causes inflammation in the microglia, so when they encounter newly formed brain cells with presenilin mutations they may overreact and kill them off prematurely. He feels that this discovery about the microglia’s role opens another important avenue toward understanding the biology of Alzheimer’s disease.
“I’ve been studying amyloid for 30 years, but there’s something else going on here, and the role of neurogenesis is really underappreciated,” he said. “This is another way to understand the biology of these genes that we know significantly affect the progression of disease and loss of memory.”
Additional authors include Sylvia Ortega-Martinez, Nisha Palla, Xiaoqiong Zhang and Erin Lipman from the University of Chicago.
Citation: “Deficits in Enrichment-Dependent Neurogenesis and Enhanced Anxiety Behaviors Mediated by Expression of Alzheimer’s Disease-Linked Ps1 Variants Are Rescued by Microglial Depletion.” Journal of Neuroscience, Aug. 21, 2019. DOI: 10.1523/JNEUROSCI.0884-19.2019
MIT engineers have developed a magnetically steerable, thread-like robot that can actively glide through narrow, winding pathways, such as the labrynthine vasculature of the brain.
In the future, this robotic thread may be paired with existing endovascular technologies, enabling doctors to remotely guide the robot through a patient’s brain vessels to quickly treat blockages and lesions, such as those that occur in aneurysms and stroke.
“Stroke is the number five cause of death and a leading cause of disability in the United States. If acute stroke can be treated within the first 90 minutes or so, patients’ survival rates could increase significantly,” says Xuanhe Zhao, associate professor of mechanical engineering and of civil and environmental engineering at MIT. “If we could design a device to reverse blood vessel blockage within this ‘golden hour,’ we could potentially avoid permanent brain damage. That’s our hope.”
Zhao and his team, including lead author Yoonho Kim, a graduate student in MIT’s Department of Mechanical Engineering, describe their soft robotic design today in the journal Science Robotics. The paper’s other co-authors are MIT graduate student German Alberto Parada and visiting student Shengduo Liu.
In a tight spot
To clear blood clots in the brain, doctors often perform an endovascular procedure, a minimally invasive surgery in which a surgeon inserts a thin wire through a patient’s main artery, usually in the leg or groin. Guided by a fluoroscope that simultaneously images the blood vessels using X-rays, the surgeon then manually rotates the wire up into the damaged brain vessel. A catheter can then be threaded up along the wire to deliver drugs or clot-retrieval devices to the affected region.
Kim says the procedure can be physically taxing, requiring surgeons, who must be specifically trained in the task, to endure repeated radiation exposure from fluoroscopy.
“It’s a demanding skill, and there are simply not enough surgeons for the patients, especially in suburban or rural areas,” Kim says.
The medical guidewires used in such procedures are passive, meaning they must be manipulated manually, and are typically made from a core of metallic alloys, coated in polymer, a material that Kim says could potentially generate friction and damage vessel linings if the wire were to get temporarily stuck in a particularly tight space.
The team realized that developments in their lab could help improve such endovascular procedures, both in the design of the guidewire and in reducing doctors’ exposure to any associated radiation.
Threading a needle
Over the past few years, the team has built up expertise in both hydrogels — biocompatible materials made mostly of water — and 3-D-printed magnetically-actuated materials that can be designed to crawl, jump, and even catch a ball, simply by following the direction of a magnet.
In this new paper, the researchers combined their work in hydrogels and in magnetic actuation, to produce a magnetically steerable, hydrogel-coated robotic thread, or guidewire, which they were able to make thin enough to magnetically guide through a life-size silicone replica of the brain’s blood vessels.
The core of the robotic thread is made from nickel-titanium alloy, or “nitinol,” a material that is both bendy and springy. Unlike a clothes hanger, which would retain its shape when bent, a nitinol wire would return to its original shape, giving it more flexibility in winding through tight, tortuous vessels. The team coated the wire’s core in a rubbery paste, or ink, which they embedded throughout with magnetic particles.
Finally, they used a chemical process they developed previously, to coat and bond the magnetic covering with hydrogel — a material that does not affect the responsiveness of the underlying magnetic particles and yet provides the wire with a smooth, friction-free, biocompatible surface.
They demonstrated the robotic thread’s precision and activation by using a large magnet, much like the strings of a marionette, to steer the thread through an obstacle course of small rings, reminiscent of a thread working its way through the eye of a needle.
The researchers also tested the thread in a life-size silicone replica of the brain’s major blood vessels, including clots and aneurysms, modeled after the CT scans of an actual patient’s brain. The team filled the silicone vessels with a liquid simulating the viscosity of blood, then manually manipulated a large magnet around the model to steer the robot through the vessels’ winding, narrow paths.
Kim says the robotic thread can be functionalized, meaning that features can be added — for example, to deliver clot-reducing drugs or break up blockages with laser light. To demonstrate the latter, the team replaced the thread’s nitinol core with an optical fiber and found that they could magnetically steer the robot and activate the laser once the robot reached a target region.
When the researchers ran comparisons between the robotic thread coated versus uncoated with hydrogel, they found that the hydrogel gave the thread a much-needed, slippery advantage, allowing it to glide through tighter spaces without getting stuck. In an endovascular surgery, this property would be key to preventing friction and injury to vessel linings as the thread works its way through.
“One of the challenges in surgery has been to be able to navigate through complicated blood vessels in the brain, which has a very small diameter, where commercial catheters can’t reach,” says Kyujin Cho, professor of mechanical engineering at Seoul National University. “This research has shown potential to overcome this challenge and enable surgical procedures in the brain without open surgery.”
And just how can this new robotic thread keep surgeons radiation-free? Kim says that a magnetically steerable guidewire does away with the necessity for surgeons to physically push a wire through a patient’s blood vessels. This means that doctors also wouldn’t have to be in close proximity to a patient, and more importantly, the radiation-generating fluoroscope.
In the near future, he envisions endovascular surgeries that incorporate existing magnetic technologies, such as pairs of large magnets, the directions of which doctors can manipulate from just outside the operating room, away from the fluoroscope imaging the patient’s brain, or even in an entirely different location.
“Existing platforms could apply magnetic field and do the fluoroscopy procedure at the same time to the patient, and the doctor could be in the other room, or even in a different city, controlling the magnetic field with a joystick,” Kim says. “Our hope is to leverage existing technologies to test our robotic thread in vivo in the next step.”
Scientists are trying to emulate the human brain since it is the ultimate computing machine. In this effort, the latest research has resulted in the development of a device which can also “forget” memories much like our brains.
It is known as a second-order memristor. It mimics the synapse of a human brain in such a manner where it stores information but then loses it slowly when it is not accessed for a long time period. The device currently does not have a practical use but this could be a stepping stone to a unique kind of neurocomputer which can perform the same functions that a human brain does. The work appears in ACS Applied Materials and Interfaces.
In an analogue neurocomputer, neurons and synapses can be replicated by the on-chip electronic components. This could help in amplifying computational speeds as well as decreasing the energy requirements of the computer.
Presently the analogue neurocomputers are not feasible as researchers need to figure out how synaptic plasticity can be also implemented in electronics. This is the technique in which the active brain synapses become strong while the inactive ones get weak resulting in fading away of memories.
Previously, memristors were produced by nanosized conductive bridges which decayed with the passing of time similar to how we forget some incidents.
Anastasia Chouprik, a physicist from the Moscow Institute of Physics and Technology(MIPT), Russia said that in the first order memristor, the problem is that the device changes its behaviour with the passage of time resulting in its breakdown. The synaptic plasticity has been implemented in a robust manner this time which sustained the change in the state of the system for 100 billion times.
A ferroelectric material, hafnium oxide was used along with electric polarisation which changes in response to an electric field. It is already used by Intel for manufacturing microchips. So it would be easier to introduce the memristors.
Researchers faced challenges in finding the proper thickness for the ferroelectric material. They found four nanometres to be the ideal thickness as a nanometre more or less would make it unsuitable for application.
The forgetfulness is implemented through an imperfection as a result of which microprocessors based on hafnium are difficult to develop. The imperfection is the defect present at the interface between hafnium oxide and silicon which results in the decrease in the memristor conductivity.
There is a long way to go as these memory cells have to be made more reliable and suitable enough to be integrated into flexible electronics. Another physicist, Vitalii Mikheev said that they would be studying the relation between several mechanisms through changing the memristor. There might be mechanisms other than ferroelectric effect which have to be studied.
August 31, 2019(updated September 2, 2019) Published by Kshitij Kumar
One method by which researchers can non-invasively analyze the human brain is by developing pea-sized clusters of brain cells called “mini-brains” in the research lab. This week, the team announced that they found human-like brainwaves from these organoids in a magnificent advancement of this field of research.
The movement and nerve tract development of mini-brains has been shown by the previous studies. Biologist Alysson Muotri along with the researchers at the University of California San Diego are the first to study and record human-like neural activity. The researchers wrote that they observed brain wave patterns similar to those of a developing human in their paper published in Cell Stem Cell. Muotri said that sophistication in the in vitro model is a step to help researchers to use mini-brains to study brain development, model diseases, and study about the evolution of the brain. Researchers are good at studying cancer and the heart but the brain has been behind the curve.
Researchers introduced pluripotent human stem cells to a nutrient-rich petri-dish intended to imitate the environment in which our own brains develop to create the technical “mini-brains” called organoids. These cells could be stimulated into building a 3D structure similar to the much smaller human brain because of the multipotential (potential to become any number of different cells) nature of the stem cells. The researchers started to observe the peak of neural activity from the network at around two months of development.
Co-author and Ph.D. student Richard Gao stated that at the beginning, they weren’t checking for parallels between their model and human infant when they began to observe these intermittent bursts of electrical activity. Gao said that they observed a notable feature in organoid oscillations that the network is inactive most of the time and explode spontaneously in every 10-20 seconds. This also occurs in preterm infants called trace discontinu where strong oscillatory transients emphasize the infant’s inactive ECG. He also said that we are very lucky to find a dataset reporting these features in the preterm infant EEG at a point where oscillations vary.
Muotri said that a machine learning algorithm has been prepared by the team to identify important features in the preterm infant EEGs and had it evaluate the cerebral organoids for similarities. It was able to calculate how many weeks the organoids had developed in the culture and could no more distinguish between the organoids and the infant EEGs between 25 and 40 weeks of the organoid’s development.
Muotri and the team clarified that the comparison between the two is not necessarily one-to-one and preterm infant EEGs have some limitations including the impact the thickness of a developing human skull has on readings which differ from the lab-produced organoids.
Arnold Kriegstein, a neurologist from the University of California, San Francisco, who did not contribute to the new study, said that it is difficult to state similarity between organoid activity and preterm EEG. The researchers have clearly shown the development of spontaneous activity in organoids to be reliable on the neuronal activity but organoids are very different from the actual developing cortex and we still need better evidence that the underlying mechanisms are the same even if the phenomenology is similar.
Muotri said that he can’t be sure whether the organoids were developed enough to be considered conscious and questions related to ethical dilemmas might be raised in the future. He intends to hold a meeting at UC San Diego with scientists, philosophers, and ethicists to talk about the ethical future of such technologies. He said that his tendency is always to say that technologies like blood transfusions or organ transplants, or even cars can be used for good as well as bad so brain organoids might also point in a similar direction in the future.
The international team of scientists from Gero Discovery LLC, the Institute of Biomedical Research of Salamanca, and Nanosyn, Inc. has found a potential drug that may prevent neuronal death through glucose metabolism modification in stressed neurons. The positive results obtained in mice are rather promising for future use in humans. The new drug can be advantageous in neurological conditions ranging from Amyotrophic lateral sclerosis, Alzheimer’s, and Huntington’s diseases to traumatic brain injury and ischemic stroke. The results have been published in theScientific Reports Journal.
Brain injuries of different nature and neurological disorders are among the most important causes of death worldwide. According to WHO, stroke is the second most common cause of mortality, and more than a third of people who have survived a stroke will have a severe disability.
What is more, as the population ages, millions of more people are posed to develop Alzheimer’s or Parkinson’s diseases in the near future. However, there are no efficient drugs for major neurodegenerative diseases. It is thus critically important to understand the biology of these diseases and to identify new drugs capable of improving quality of life, survival, and, in the best-case scenario, curing the disease completely.
Glycolysis is generally considered as the metabolic pathway essential for cell survival since it meets cell energy needs in case of intensive energy consumption. However, it is already known that in the brain tissue, the situation is quite different – different cell types show distinct glucose metabolism patterns. In neurons, only a small portion of glucose is consumed via the glycolysis pathway. At the same time, astrocytes provide nutrients to neurons and utilize glycolysis to metabolize glucose. These differences are mostly due to the special protein called PFKFB3, which is normally absent in neurons and is active in astrocytes. In the case of certain neurological diseases, stroke being one of them, the amount of active PFKFB3 increases in neurons, which is highly stressful for these cells and leads to cell death.
An international team of researchers led by Peter Fedichev, a scientist and biotech entrepreneur from Gero Discovery, and professor Juan P. Bolaños from the University of Salamanca, suggested and further confirmed in the in vivo experiments that a small molecule, the inhibitor of PFKFB3, may prevent cell death in the case of ischemia injury. Inhibition of PFKFB3 improves motor coordination of mice after stroke and reduced brain infarct volume. Moreover, in the experiments using mouse cell cultures, it was shown that PFKFB3 inhibitor protects neurons from the amyloid-beta peptide, the main component of the amyloid plaques found in the brains of Alzheimer’s disease patients.
Professor Juan P. Bolaños: “Excitotoxicity is a hallmark of various neurological diseases, stroke being one of them. Our group has previously established a link between this pathological condition and high activity of PFKFB3 enzyme in neurons, which leads to severe oxidative stress and neuronal death“
“We are glad that our hypothesis that pharmacological inhibition of PFKFB3 can be beneficial in an excitotoxicity-related condition, such as stroke was confirmed. I would like to note that In our work, we used a known molecule to demonstrate that PFKFB3 blockage has a therapeutic effect. But, we have also performed the same experiments with other proprietary small molecule designed in our company and showed that it had a similar effect. There is, of course, still much work to do. We are currently investigating the efficacy of our compounds in the models of orphan excitotoxicity-related neurological diseases. We have already obtained good safety results in mice and believe that we will be successful in our future investigations” said Olga Burmistrova, Director of preclinical development in Gero Discovery.
Gero Discovery team is planning to proceed with preclinical trials and to move into clinical trials soon. “These promising results bring hope to dozens of millions of patients suffering from life-threatening neurological diseases and provide tremendous business opportunities in many indications with unmet needs. We start communicating with potential investors and co-development partners and invite interested parties to collaborate on the further development of this breakthrough medicine through the preclinical and early clinical stage” mentioned Maksim Kholin, the Gero Discovery Co-Founder and Business Development Director.
August 26, 2019(updated August 26, 2019) Published by Sai Teja
It often happens that we can remember something which occurred long back but forget the incident that took place recently. Some memories remain stable while others fade away in minutes.
Researchers from Caltech have found that the memories which remain stable over time are encoded by a group of neurons firing in synchrony thus providing redundancy. The work also tries to understand the effects on memory after tragic events such as brain damage or Alzheimer’s disease.
The experiments were carried out in the laboratory of Carlos Lois, a biology professor and affiliated faculty member of Tianqiao and Chrissy Chen Institute for Neuroscience. It appears in the Science journal.
The team was led by Walter Gonzalez, a postdoc scholar. A test was developed for testing the neural activity of mice when they learn and remember a new place. The mouse was kept in a straight enclosure of length 5 feet. Different symbols were marked in different locations on the walls such as a bold plus sign at the rightmost end and angled slash close to the center. Sugar water was placed at the track ends. As the mouse explored places, the activities of certain neurons in the hippocampuswere tracked by the scientists.
When initially placed in the track, the mouse wandered till it found the sugar water. Single neurons were activated when it spotted a symbol on the wall. However, on staying longer, the mouse remembered the sugar locations. As the familiarity increased more neurons got activated in synchrony as it spotted the symbols.
To understand the fading of memories, the mice were kept away from the track for 20 days. On getting back to the track, the mice which had strong memories encoded by high numbers of neurons remembered the task easily. So when large groups of neurons encode an activity, the memories can be easily recalled even if some showed different activity or remained silent.
This can be explained in a way similar to how a long story is remembered. For remembering a long story, it can be told to many different people and when all of them gather each can fill in the gaps which the other member has forgotten. By repeating this every time, the story can be preserved with the strengthening of the memory. In a similar way, neurons help each other in encoding memories which stay over time.
Impairment of memory in any form can affect us a lot since our life is basically driven by memories. Senior citizens get affected by this as a part of the aging process. Alzheimer’s disease also has devastating effects which paralyze even the basic daily functioning of a person. When memory is encoded by fewer neurons it can be forgotten easily. As a result of this, treatments which increase the recruitment of a large number of neurons for encoding a memory help in preventing memory loss.
When an activity is practiced a lot, there are more chances of remembering it as more neurons are encoded for the action. It is usually considered that to make a memory stable, individual connections to a neuron have to be strengthened. However, the study suggests that the memory can be stored for a long period of time with an increase in the neurons which encode it.
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