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A team of academic researchers has identified the intracellular mechanisms regulated by vitamin D3 that may help the body clear the brain of amyloid beta, the main component of plaques associated with Alzheimer's disease.

Published in the March 6 issue of the Journal of Alzheimer's Disease, the early findings show that vitamin D3 may activate key genes and cellular signaling networks to help stimulate the immune system to clear the amyloid-beta protein.

Previous laboratory work by the team demonstrated that specific types of immune cells in Alzheimer's patients may respond to therapy with vitamin D3 and curcumin, a chemical found in turmeric spice, by stimulating the innate immune system to clear amyloid beta. But the researchers didn't know how it worked.

"This new study helped clarify the key mechanisms involved, which will help us better understand the usefulness of vitamin D3 and curcumin as possible therapies for Alzheimer's disease," said study author Dr. Milan Fiala, a researcher at the David Geffen School of Medicine at UCLA and the Veterans Affairs Greater Los Angeles Healthcare System.

For the study, scientists drew blood samples from Alzheimer's patients and healthy controls and then isolated critical immune cells from the blood called macrophages, which are responsible for gobbling up amyloid beta and other waste products in the brain and body.

The team incubated the immune cells overnight with amyloid beta. An active form of vitamin D3 called 1a,25–dihydroxyvitamin D3, which is made in the body by enzymatic conversion in the liver and kidneys, was added to some of the cells to gauge the effect it had on amyloid beta absorption.

Previous work by the team, based on the function of Alzheimer's patients' macrophages, showed that there are at least two types of patients and macrophages: Type I macrophages are improved by addition of 1a,25–dihydroxyvitamin D3 and curcuminoids (a synthetic form of curcumin), while Type II macrophages are improved only by adding 1a,25–dihydroxyvitamin D3.

Researchers found that in both Type I and Type II macrophages, the added 1a,25–dihydroxyvitamin D3 played a key role in opening a specific chloride channel called "chloride channel 3 (CLC3)," which is important in supporting the uptake of amyloid beta through the process known as phagocytosis. Curcuminoids activated this chloride channel only in Type I macrophages.

The scientists also found that 1a,25–dihydroxyvitamin D3 strongly helped trigger the genetic transcription of the chloride channel and the receptor for 1a,25–dihydroxyvitamin D3 in Type II macrophages. Transcription is the first step leading to gene expression.

The mechanisms behind the effects of 1a,25–dihydroxyvitamin D3 on phagocytosis were complex and dependent on calcium and signaling by the "MAPK" pathway, which helps communicate a signal from the vitamin D3 receptor located on the surface of a cell to the DNA in the cell's nucleus.

The pivotal effect of 1a,25–dihydroxyvitamin D3 was shown in a collaboration between Dr. Patrick R. Griffin from the Scripps Research Institute and Dr. Mathew T. Mizwicki from UC Riverside. They utilized a technique based on mass spectrometry, which showed that 1a,25–dihydroxyvitamin D3 stabilized many more critical sites on the vitamin D receptor than did the curcuminoids.

"Our findings demonstrate that active forms of vitamin D3 may be an important regulator of immune activities of macrophages in helping to clear amyloid plaques by directly regulating the expression of genes, as well as the structural physical workings of the cells," said study author Mizwicki, who was an assistant research biochemist in the department of biochemistry at UC Riverside when the study was conducted.

According to the team, one of the next stages of research would be a clinical trial with vitamin D3 to assess the impact on Alzheimer's disease patients. Previous studies by other teams have shown that a low serum level of 25–hydroxyvitamin D3 may be associated with cognitive decline. It is too early to recommend a definitive dosage of vitamin D3 to help with Alzheimer's disease and brain health, the researchers said.

The study was funded in part by the Alzheimer's Association and by the National Institutes of Health.

Other study authors included Danusa Menegaz and Antonio Barrientos-Duran of the department of biochemistry at UC Riverside; Jun Zhang and Patrick R. Griffin of the department of molecular therapeutics at the Scripps Research Institute in Jupiter, Fla.; Stephen Tse of the department of medicine at the David Geffen School of Medicine at UCLA and the Veterans Affairs Greater Los Angeles Healthcare System; and John R. Cashman of the Human BioMolecular Research Institute in San Diego, Calif.

Source: UCLA Health System

  • "It is too early to recommend a definitive dosage of vitamin D3 to help with Alzheimer's disease and brain health, the researchers said." Right! Don't want to interfere w/ any new patent drugs that might be coming out of big pharma.
    Since D3 has a low order of toxicity 5000 iu/d cholecalciferol would be a reasonable and very safe starting point. This will normalize the blood level to ca. 50 ng/ml in several months.

Parkinson's Disease Stopped in Animal Model

Featured In: Disease Research | Academia News

Friday, March 2, 2012

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Millions of people suffer from Parkinson's disease, a disorder of the nervous system that affects movement and worsens over time. As the world's population ages, it's estimated that the number of people with the disease will rise sharply. Yet despite several effective therapies that treat Parkinson's symptoms, nothing slows its progression.

While it's not known what exactly causes the disease, evidence points to one particular culprit: a protein called α-synuclein. The protein, which has been found to be common to all patients with Parkinson's, is thought to be a pathway to the disease when it binds together in "clumps," or aggregates, and becomes toxic, killing the brain's neurons.

Now, scientists at UCLA have found a way to prevent these clumps from forming, prevent their toxicity and even break up existing aggregates.

UCLA professor of neurology Jeff Bronstein and UCLA associate professor of neurology Gal Bitan, along with their colleagues, report the development of a novel compound known as a "molecular tweezer," which in a living animal model blocked α-synuclein aggregates from forming, stopped the aggregates' toxicity and, further, reversed aggregates in the brain that had already formed. And the tweezers accomplished this without interfering with normal brain function.

The research appears in the online edition of the journal Neurotherapeutics.

There are currently more than 30 diseases with no cure that are caused by protein aggregation and the resulting toxicity to the brain or other organs, including Parkinson's, Alzheimer's and Type 2 diabetes. It is therefore critical, Bronstein said, to find a way to stop this aggregation process. Over the last two decades, researchers and pharmaceutical companies have attempted to develop drugs that would prevent abnormal protein aggregation, but so far, they have had little or no success.

While these aggregates are a natural target for a drug, finding a therapy that targets only the aggregates is a complicated process, Bronstein said. In Parkinson's, for example, the protein implicated in the disorder, α-synuclein, is naturally ubiquitous throughout the brain.

"Its normal function is not well understood, but it may play a role in aiding communication between neurons," Bronstein said. "The trick, then, is to prevent the α-synuclein protein aggregates and their toxicity without destroying α-synuclein's normal function, along with, of course, other healthy areas of the brain.

Molecular tweezer
Bronstein collaborated with Bitan, who had been working with a particular molecular tweezer he had developed called CLR01. Molecular tweezers are complex molecular compounds that are capable of binding to other proteins. Shaped like the letter "C," these compounds wrap around chains of lysine, a basic amino acid that is a constituent of most proteins.

Working first in cell cultures, the researchers found that CLR01 was able to prevent α-synuclein from forming aggregates, prevent toxicity and even break up existing aggregates.

"The most surprising aspect of the work," Bronstein said, "is that despite the ability of the compound to bind to many proteins, it did not show toxicity or side effects to normal, functioning brain cells."

"We call this unique mechanism 'process-specific,' rather than the common protein-specific inhibition," Bitan added, meaning the compound only attacked the targeted aggregates and nothing else.

The researchers next tried their tweezers in a living animal, the zebrafish, a tropical freshwater fish commonly found in aquariums. The zebrafish is a popular animal for research because it is easily manipulated genetically, develops rapidly and is transparent, making the measurement of biological processes easier.

Using a transgenic zebrafish model for Parkinson's disease, the researchers added CLR01 and used fluorescent proteins to track the tweezer's effect on the aggregations. They found that, just as in cell cultures, CLR01 prevented α-synuclein aggregation and neuronal death, thus stopping the progression of the disorder in the living animal model.

Being able to prevent α-synuclein from aggregating, prevent toxicity and break up existing aggregates is a very encouraging result, but still, at the end of the day, "we've only stopped Parkinson's in zebrafish," Bronstein said.

"Nonetheless," he said, "all of these benefits of CLR01 were found without any evidence of toxicity. And taken together, CLR01 holds great promise as a new drug that can slow or stop the progression of Parkinson's and related disorders. This takes us one step closer to a cure."

The researchers are already studying CLR01 in a mouse model of Parkinson's and say they hope this will lead to human clinical trials.

Source: University of California, Los Angeles

 

Consuming Flavanol-rich Cocoa May Enhance Brain Function

Featured In: Academia News | Neuroscience

Tuesday, August 14, 2012

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Eating cocoa flavanols External link daily may improve mild cognitive impairment, according to new research in the American Heart Association’s journal Hypertension.

Each year, more than six percent of people aged 70 years or older develop mild cognitive impairment, a condition involving memory loss that can progress to dementia and Alzheimer’s disease.

Flavanols can be found in tea, grapes, red wine, apples and cocoa products and have been associated with a decreased risk of dementia. They may act on the brain structure and function directly by protecting neurons from injury, improving metabolism and their interaction with the molecular structure responsible for memory researchers said. Indirectly, flavAnols may help by improving brain blood flow.

In this study, 90 elderly participants with mild cognitive impairment were randomized to drink daily either 990 milligrams (high), 520 mg (intermediate) or 45 mg (low) of a dairy-based cocoa flavanol drink for eight weeks. The diet was restricted to eliminate other sources of flavanols from foods and beverages other than the dairy-based cocoa drink.

Cognitive function was examined by neuro-psychological tests of executive function, working memory, short-term memory, long-term episodic memory, processing speed and global cognition.

Researchers found:

“This study provides encouraging evidence that consuming cocoa flavanols, as a part of a calorie-controlled and nutritionally-balanced diet, could improve cognitive function,” said Giovambattista Desideri, M.D., study lead author and director of Geriatric Division, Department of Life, Health and Environmental Sciences, University of L’Aquila in Italy. “The positive effect on cognitive function may be mainly mediated by an improvement in insulin sensitivity. It is yet unclear whether these benefits in cognition are a direct consequence of cocoa flavanols or a secondary effect of general improvements in cardiovascular function.”

The study population was generally in good health without known cardiovascular disease. Thus, it would not be completely representative of all mild cognitive impairment patients. In addition, only some clinical features of mild cognitive impairment were explored in the study.

“Given the global rise in cognitive disorders, which have a true impact on an individual’s quality of life, the role of cocoa flavanols in preventing or slowing the progression of mild cognitive impairment to dementia warrants further research,” Desideri said. “Larger studies are needed to validate the findings, figure out how long the positive effects will last and determine the levels of cocoa flavanols required for benefit.”

Source: American Heart Association

 

Scientists Discover How the Brain Ages

Featured In: Editor's Picks | Academia News | Neuroscience | Europe

Wednesday, September 12, 2012
 

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Researchers at Newcastle University have revealed the mechanism by which neurons, the nerve cells in the brain and other parts of the body, age. The research, published in Aging Cell, opens up new avenues of understanding for conditions where the aging of neurons are known to be responsible, such as dementia and Parkinson’s disease.

The aging process has its roots deep within the cells and molecules that make up our bodies. Experts have previously identified the molecular pathway that react to cell damage and stems the cell’s ability to divide, known as cell senescence.

However, in cells that do not have this ability to divide, such as neurons in the brain and elsewhere, little was understood of the ageing process. Now a team of scientists at Newcastle University, led by Professor Thomas von Zglinicki have shown that these cells follow the same pathway.

This challenges previous assumptions on cell senescence and opens new areas to explore in terms of treatments for conditions such as dementia, motor neuron disease or age-related hearing loss.

Newcastle University’s Professor Thomas von Zglinicki who led the research said: “We want to continue our work looking at the pathways in human brains as this study provides us with a new concept as to how damage can spread from the first affected area to the whole brain.”

Working with the University’s special colony of aged mice, the scientists have discovered that ageing in neurons follows exactly the same rules as in senescing fibroblasts, the cells which divide in the skin to repair wounds.

DNA damage responses essentially re-program senescent fibroblasts to produce and secrete a host of dangerous substances including oxygen free radicals or reactive oxygen species (ROS) and pro-inflammatory signalling molecules. This makes senescent cells the ‘rotten apple in a basket’ that can damage and spoil the intact cells in their neighbourhood. However, so far it was always thought that ageing in cells that can’t divide - post-mitotic, non-proliferating cells - like neurons would follow a completely different pathway.

Now, this research explains that in fact ageing in neurons follows exactly the same rules as in senescing fibroblasts.

Professor von Zglinicki, professor of Cellular Gerontology at Newcastle University said: “We will now need to find out whether the same mechanisms we detected in mouse brains are also associated with brain ageing and cognitive loss in humans. We might have opened up a short-cut towards understanding brain ageing, should that be the case.”

Dr Diana Jurk, who did most of this work during her PhD in the von Zglinicki group, said: “It was absolutely fascinating to see how ageing processes that we always thought of as completely separate turned out to be identical. Suddenly so much disparate knowledge came together and made sense.”

The research contributes to the Newcastle Initiative on Changing Age, the University’s response to the societal challenge of Ageing, seeking new ways to make the most of the extensive opportunities associated with increasing human longevity.

The team want to further study the mechanism using the unique resource of the Newcastle Brain Bank.

Source: Newcastle University

 

Rebuilding the Brain’s Circuitry Featured In: Academia News | Neuroscience Monday, November 28, 2011
Neuron transplants have repaired brain circuitry and substantially normalized function in mice with a brain disorder, an advance indicating that key areas of the mammalian brain are more reparable than was widely believed. Collaborators from Harvard University, Massachusetts General Hospital (MGH), Beth Israel Deaconess Medical Center (BIDMC) and Harvard Medical School (HMS) transplanted normally functioning embryonic neurons at a carefully selected stage of their development into the hypothalamus of mice unable to respond to leptin, a hormone that regulates metabolism and controls body weight. These mutant mice usually become morbidly obese, but the neuron transplants repaired defective brain circuits, enabling them to respond to leptin and thus experience substantially less weight gain. Repair at the cellular-level of the hypothalamus — a critical and complex region of the brain that regulates phenomena such as hunger, metabolism, body temperature, and basic behaviors such as sex and aggression — indicates the possibility of new therapeutic approaches to even higher-level conditions such as spinal cord injury, autism, epilepsy, ALS (Lou Gehrig’s disease), Parkinson’s disease, and Huntington’s disease. “There are only two areas of the brain that are known to normally undergo ongoing large-scale neuronal replacement during adulthood on a cellular level — so-called ‘neurogenesis,’ or the birth of new neurons — the olfactory bulb and the subregion of the hippocampus called the dentate gyrus, with emerging evidence of lower level ongoing neurogenesis in the hypothalamus,” said Jeffrey Macklis, Harvard University professor of stem cell and regenerative biology and HMS professor of neurology at MGH, and one of three corresponding authors on the paper. “The neurons that are added during adulthood in both regions are generally smallish and are thought to act a bit like volume controls over specific signaling. Here we’ve rewired a high-level system of brain circuitry that does not naturally experience neurogenesis, and this restored substantially normal function.” The two other senior authors on the paper are Jeffrey Flier, dean of Harvard Medical School, and Matthew Anderson, HMS professor of pathology at BIDMC. The findings are to appear Nov. 25 in Science. In 2005, Flier, then the George C. Reisman professor of medicine at BIDMC, published a landmark study, also in Science, showing that an experimental drug spurred the addition of new neurons in the hypothalamus and offered a potential treatment for obesity. But while the finding was striking, the researchers were unsure whether the new cells functioned like natural neurons. Macklis’ laboratory had for several years developed approaches to successfully transplanting developing neurons into circuitry of the cerebral cortex of mice with neurodegeneration or neuronal injury. In a landmark 2000 Nature study, the researchers demonstrated induction of neurogenesis in the cerebral cortex of adult mice, where it does not normally occur. While these and follow-up experiments appeared to rebuild brain circuitry anatomically, the new neurons’ level of function remained uncertain. To learn more, Flier, an expert in the biology of obesity, teamed up with Macklis, an expert in central nervous system development and repair, and Anderson, an expert in neuronal circuitries and mouse neurological disease models. The groups used a mouse model in which the brain lacks the ability to respond to leptin. Flier and his lab have long studied this hormone, which is mediated by the hypothalamus. Deaf to leptin’s signaling, these mice become dangerously overweight. Prior research had suggested that four main classes of neurons enabled the brain to process leptin signaling. Postdocs Artur Czupryn and Maggie Chen, from Macklis’ and Flier’s labs, respectively, transplanted and studied the cellular development and integration of progenitor cells and very immature neurons from normal embryos into the hypothalamus of the mutant mice using multiple types of cellular and molecular analysis. To place the transplanted cells in exactly the correct and microscopic region of the recipient hypothalamus, they used a technique called high-resolution ultrasound microscopy, creating what Macklis called a “chimeric hypothalamus” — like the animals with mixed features from Greek mythology. Postdoc Yu-Dong Zhou, from Anderson’s lab, performed in-depth electrophysiological analysis of the transplanted neurons and their function in the recipient circuitry, taking advantage of the neurons’ glowing green from a fluorescent jellyfish protein carried as a marker. These nascent neurons survived the transplantation process and developed structurally, molecularly, and electrophysiologically into the four cardinal types of neurons central to leptin signaling. The new neurons integrated functionally into the circuitry, responding to leptin, insulin, and glucose. Treated mice matured and weighed approximately 30 percent less than their untreated siblings or siblings treated in multiple alternate ways. The researchers then investigated the precise extent to which these new neurons had become wired into the brain’s circuitry using molecular assays, electron microscopy for visualizing the finest details of circuits, and patch-clamp electrophysiology, a technique in which researchers use small electrodes to investigate the characteristics of individual neurons and pairs of neurons in fine detail. Because the new cells were labeled with fluorescent tags, postdocs Czupryn, Zhou, and Chen could easily locate them. The Zhou and Anderson team found that the newly developed neurons communicated to recipient neurons through normal synaptic contacts, and that the brain, in turn, signaled back. Responding to leptin, insulin and glucose, these neurons had effectively joined the brain’s network and rewired the damaged circuitry. “It’s interesting to note that these embryonic neurons were wired in with less precision than one might think,” Flier said. “But that didn’t seem to matter. In a sense, these neurons are like antennas that were immediately able to pick up the leptin signal. From an energy-balance perspective, I’m struck that a relatively small number of genetically normal neurons can so efficiently repair the circuitry.” “The finding that these embryonic cells are so efficient at integrating with the native neuronal circuitry makes us quite excited about the possibility of applying similar techniques to other neurological and psychiatric diseases of particular interest to our laboratory,” said Anderson. The researchers call their findings a proof of concept for the broader idea that new neurons can integrate specifically to modify complex circuits that are defective in a mammalian brain. The researchers are interested in further investigating controlled neurogenesis — directing growth of new neurons in the brain from within — the subject of much of Macklis’ research as well as Flier’s 2005 paper, and a potential route to new therapies. “The next step for us is to ask parallel questions of other parts of the brain and spinal cord, those involved in ALS and with spinal cord injuries,” Macklis said. “In these cases, can we rebuild circuitry in the mammalian brain? I suspect that we can.”
    This study was funded by the National Institutes of Health, the Jane and Lee Seidman Fund for Central Nervous System Research, the Emily and Robert Pearlstein Fund for Nervous System Repair, the Picower Foundation, the National Institute of Neurological Disorders and Stroke, Autism Speaks, and the Nancy Lurie Marks Family Foundation. Source: Harvard University

New findings, led by neuroscientists at the University of Bristol and published this week in the journal Neurobiology of Aging, reveal a novel mechanism through which the brain may become more reluctant to function as we grow older.

It is not fully understood why the brain’s cognitive functions such as memory and speech decline as we age. Although work published this year suggests cognitive decline can be detectable before 50 years of age. The research, led by Professor Andy Randall and Dr Jon Brown from the University’s School of Physiology and Pharmacology, identified a novel cellular mechanism underpinning changes to the activity of neurones which may underlie cognitive decline during normal healthy aging.

The brain largely uses electrical signals to encode and convey information. Modifications to this electrical activity are likely to underpin age-dependent changes to cognitive abilities.

The researchers examined the brain’s electrical activity by making recordings of electrical signals in single cells of the hippocampus, a structure with a crucial role in cognitive function. In this way they characterised what is known as “neuronal excitability” — this is a descriptor of how easy it is to produce brief, but very large, electrical signals called action potentials; these occur in practically all nerve cells and are absolutely essential for communication within all the circuits of the nervous system.

Action potentials are triggered near the neurone’s cell body and once produced travel rapidly through the massively branching structure of the nerve cell, along the way activating the synapses the nerve cell makes with the numerous other nerve cells to which it is connected.

The Bristol group identified that in the aged brain it is more difficult to make hippocampal neurones generate action potentials. Furthermore they demonstrated that this relative reluctance to produce action potential arises from changes to the activation properties of membrane proteins called sodium channels, which mediate the rapid upstroke of the action potential by allowing a flow of sodium ions into neurones.

Professor Randall, Professor in Applied Neurophysiology said: “Much of our work is about understanding dysfunctional electrical signalling in the diseased brain, in particular Alzheimer’s disease. We began to question, however, why even the healthy brain can slow down once you reach my age. Previous investigations elsewhere have described age-related changes in processes that are triggered by action potentials, but our findings are significant because they show that generating the action potential in the first place is harder work in aged brain cells.

"Also by identifying sodium channels as the likely culprit for this reluctance to produce action potentials, our work even points to ways in which we might be able modify age-related changes to neuronal excitability, and by inference cognitive ability.”

The research, entitled ‘Age-related changes to Na+ channel gating contribute to modified intrinsic neuronal excitability’ by Andrew D Randall, Clair Booth and Jon T Brown, is published in the journal Neurobiology of Aging and funded by Pfizer who are long-standing collaborators with Randall and Brown.
Andrew D. Randall, Clair Booth, Jon T. Brown. Age-related changes to Na channel gating contribute to modified intrinsic neuronal excitability. Neurobiology of Aging, 2012; DOI: 10.1016/j.neurobiolaging.2011.12.030

Source: University of Bristol

Aging impairs intermediate-term behavioral memory by disrupting the dorsal paired medial neuron memory trace

  1. Ronald L. Davis1

+ Author Affiliations

  1. Department of Neuroscience, The Scripps Research Institute Florida, Jupiter, FL 33458
  1. Edited by Leslie C. Griffith, Brandeis University, Waltham, MA, and accepted by the Editorial Board March 14, 2012 (received for review November 4, 2011)

Abstract

How the functional activity of the brain is altered during aging to cause age-related memory impairments is unknown. We used functional cellular imaging to monitor two different calcium-based memory traces that underlie olfactory classical conditioning in young and aged Drosophila. Functional imaging of neural activity in the processes of the dorsal paired medial (DPM) and mushroom body neurons revealed that the capacity to form an intermediate-term memory (ITM) trace in the DPM neurons after learning is lost with age, whereas the capacity to form a short-term memory trace in the α′/β′ mushroom body neurons remains unaffected by age. Stimulation of the DPM neurons by activation of a temperature-sensitive cation channel between acquisition and retrieval enhanced ITM in aged but not young flies. These data indicate that the functional state of the DPM neurons is selectively altered with age to cause an age-related impairment of ITM, and demonstrate that altering the excitability of DPM neurons can restore age-related memory impairments.

Footnotes

Brain Cells can be Made from Skin Cells

March 1, 2012

Cambridge scientists have, created cerebral cortex cells – those that make up the brain’s gray matter – from a small sample of human skin. The researchers’ findings, which were funded by Alzheimer’s Research UK and the Wellcome Trust, were published in Nature Neuroscience.

Diseases of the cerebral cortex range from developmental conditions, such as epilepsy and autism, to neurodegenerative conditions such as Alzheimer’s. Today’s findings will enable scientists to study how the human cerebral cortex develops, how it "wires up" and how that can go wrong (a common problem leading to learning disabilities).



It will also allow them to recreate brain diseases, such as Alzheimer’s, in the lab. This will give them previously impossible insight, allowing them to both watch the diseases develop in real time and also develop and test new drugs to stop the diseases progressing.

Rick Livesey of the Gurdon Institute and Department of Biochemistry at the Univ. of Cambridge, principal investigator of the research, says, “This approach gives us the ability to study human brain development and disease in ways that were unimaginable even five years ago.”

For their research, the scientists took skin biopsies from patients and then reprogrammed the cells from the skin samples back into stem cells. These stem cells as well as human embryonic stem cells were then used to generate cerebral cortex cells.

Livesey adds, “We are using this system to recreate Alzheimer’s disease in the lab. Alzheimer’s disease is the commonest form of dementia in the world, and dementia currently affects over 800,000 people in the UK. It’s a disease that primarily affects the type of nerve cell we’ve made in the lab, so we’ve the perfect tool to create a full, human model of the disease in the lab.”

Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, says, “We are really pleased to have contributed funding for this work and the results are a positive step forward. Turning stem cells into networks of fully functional nerve cells in the lab holds great promise for unraveling complex brain diseases such as Alzheimer’s. Dementia is the greatest medical challenge of our time – we urgently need to understand more about the condition and how to stop it. We hope these findings can move us closer towards this goal.”

This is a beautiful image of human brain cells, which can now be grown from adult skin cells. The brain neural stem cells were derived from human skin cells. These stem cells express typical marker genes of brain neocortical stem cells, such as Pax6 labeled here with red fluorescent. They form a rosette structure resembling the transection of the neural tube. The entire image is about 250 µm across (a really thick bit of human hair).

Source: Cambridge
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