TAG: "Huntington’s disease"

UC researchers awarded stem cell grants


Funding to develop treatments for Huntington’s, spina bifida, chronic diabetic wounds.

Roslyn Rivkah Isseroff, UC Davis

University of California researchers from two campuses received three grants totaling more than $12 million in funding from the state’s stem cell agency to develop stem cell treatments for Huntington’s disease, spina bifida and chronic diabetic wounds.

The funding was part of $25.2 million in Preclinical Development Awards targeting seven deadly or disabling disorders – what the California Institute for Regenerative Medicine considers “the most promising” research leading up to human clinical trials using stem cells to treat disease and injury.

UC Davis researchers were awarded a pair of grants totaling more than $7 million to develop stem cell therapies for spina bifida ($2.2 million) and chronic diabetic wounds ($5 million).

Diana Farmer, professor and chair of surgery at UC Davis Medical Center, is developing a placental stem cell therapy for spina bifida, the common and devastating birth defect that causes lifelong paralysis as well as bladder and bowel incontinence. She and her team are working on a unique treatment that can be applied in utero – before a baby is born — in order to reverse spinal cord damage.

Diana Farmer, UC Davis

Roslyn Rivkah Isseroff, a UC Davis professor of dermatology, and Jan Nolta, professor of internal medicine and director of the university’s Stem Cell Program, are developing a wound dressing containing stem cells that could be applied to chronic wounds and be a catalyst for rapid healing. This is Isseroff’s second CIRM grant, and it will help move her research closer to having a product approved by the U.S. Food and Drug Administration that specifically targets diabetic foot ulcers, a condition affecting more than 6 million people in the country.

Also, Leslie Thompson of the Sue & Bill Gross Stem Cell Research Center at UC Irvine has been awarded $5 million to continue her CIRM-funded effort to develop stem cell treatments for Huntington’s disease. The grant supports her next step: identifying and testing stem cell-based treatments for HD, an inherited, incurable and fatal neurodegenerative disorder. In this project, Thompson and her colleagues will create an HD therapy employing human embryonic stem cells that can be evaluated in clinical trials.

Leslie Thompson, UC Irvine

CIRM’s governing board also approved an application for the Tools and Technology Award that had been deferred from the January meeting. UCLA’s Carla Koehler will now get $1.3 million for research on a small molecule tool for reducing the malignant potential in reprogramming human induced pluripotent stem cells and embryonic stem cells.

Overall, CIRM’s governing board has awarded nearly $1.9 billion in stem cell grants, with half of the total going to the University of California or UC-affiliated institutions.

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UC Davis Huntington’s Disease Center receives Level 1 designation


Joins UCLA, UC San Diego as one of 21 centers designated by Huntington’s Disease Society.

By Phyllis Brown, UC Davis

The UC Davis Huntington’s Disease Center, whose compassionate patient care and research expertise have made it a beacon of hope for people with Huntington’s disease throughout Northern California and beyond, has been acknowledged by the national society committed to the values that it so ably upholds  the Huntington’s Disease Society of America — as a Level 1 Huntington’s Disease Center of Excellence.

The acknowledgement recognizes the center’s service to over 300 families coping with Huntington’s disease and its plan to provide both medical and social services to a large number of underserved families coping with Huntington’s disease who are affiliated with Kaiser Permanente in Northern California.

Huntington’s disease is an inherited, degenerative brain disorder for which there is no cure and only one Food and Drug Administration-approved treatment, Xenazine (tetra benazine). The condition slowly diminishes the affected individual’s ability to walk, talk and reason. They eventually become completely dependent upon others for their care.

“The Huntington’s Disease Society of America was impressed with the scope of UC Davis’ plan to provide expert care to the large number of underserved families who use the Kaiser Permanente insurance system,” said Louise Vetter, chief executive officer of the Huntington’s Disease Society of America. “UC Davis has our continued thanks for the center’s support of the Huntington’s Disease Society of America’s mission and all that it does to provide exemplary care to families impacted by Huntington’s disease.”

The UC Davis Huntington’s Disease clinic has been designated as one of 21 Huntington’s Disease Centers of Excellence in the United States since 2001. There are three other centers of excellence in the western United States, at UCLA, UC San Diego and the University of Washington in Seattle, which is also a Level 1 center.

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Molecular ‘switch’ ID’d that causes Huntington’s-like symptoms in mice


UCLA finding provides clues to how disease develops.

A mouse explores blocks that symbolize the first 17 amino acids of the protein huntingtin that, when mutated, causes Huntington’s disease. (Photo by Yang Lab, UCLA)

By Mark Wheeler, UCLA

Scientists know that Huntington’s disease is caused by an inherited gene mutation. But research has yet to identify the specific mechanisms that trigger the disease and cause it to advance — and there is currently no way to prevent the disease or slow its progression.

Now, researchers at UCLA have found that removing a specific molecular switch from a mutant protein can trigger symptoms in mice that are similar to those found in people with Huntington’s disease. The finding provides further insight into how the disease evolves.

The study, led by X. William Yang, a UCLA professor of psychiatry, appears in the current online edition of the journal Neuron.

Huntington’s disease affects 1 in every 10,000 Americans while another 250,000 are at risk because they carry the inherited gene mutation. That mutation leads to an extra-long stretch of amino acids called glutamine in the huntingtin protein.

Symptoms include chorea (jerky, uncontrollable movements), dystonia (sustained involuntary muscle contractions) and an abnormal gait that can cause frequent falls. People with Huntington’s also suffer from debilitating cognitive and psychiatric deficits and they typically die of complications from the disease about 20 years after the onset of symptoms. Most of those who have Huntington’s disease do not show symptoms until middle age, meaning that many unknowingly pass on the mutated gene to their children.

In 2009, Yang and his colleagues genetically manipulated a small domain on the huntingtin protein called N17 that is located immediately before the mutant glutamine stretch. In doing so they found they could dramatically suppress the disease in an earlier mouse model of Huntington’s disease they had developed.

That led them to the question that framed their latest study: If the N17 domain could alter the mutant huntingtin for the good, what would happen if the N17 domain function were completely abolished?

To find the answer, the scientists developed a new mouse model with the N17 domain removed altogether, allowing them to dissect the molecular function of that part of the protein that causes the disease in mice.

“Although we did expect the mouse model to exhibit somewhat more severe disease symptoms compared to our previous Huntington’s disease mice, we were surprised to discover that deleting the domain in the new mice caused multiple disease-like symptoms and neuronal cell loss that are reminiscent of those found in Huntington’s patients,” said Dr. Xiaofeng Gu, the study’s first author and an assistant researcher in Yang’s lab.

These symptoms, which also strike in adulthood for the mice, included chorea-like and dystonia-like movement deficits, progressively worsening gait with spontaneous falls, and atrophy and neuronal cell loss in a specific brain regions, all very similar to what would be expected in people with adult-onset Huntington’s.

This new model provides important clues regarding how a normally functioning N17 domain might protect neurons in the brain against the disease, Yang said. Compared to similar mice with an intact N17 domain, the mice lacking N17 showed a markedly faster accumulation of mutant huntingtin, which appears as aggregated clumps in the nuclei of brain cells.

“This study makes clear that a major neuroprotective function of N17 is to prevent the mutant protein from entering the nucleus and eliciting more severe toxicities,” Yang said, adding that the result is consistent with findings from several studies of other, related disorders in which mutant proteins with expanded glutamine in the nucleus are key for jump-starting a disease.

The researchers also found that the mice in the study experienced inflammation in the brain somewhat similar to that found in people with Huntington’s.

“Neuroinflammation is emerging as a potentially shared mechanism in multiple neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis, and the mouse model shows similar inflammation to that found in both Huntington’s and Alzheimer’s,” Yang said. “So these mice may have the potential to be used to study disease mechanisms and test neuroprotective or anti-inflammatory therapeutics for these various disorders.”

Next, the researchers will focus on understanding the detailed molecular pathways that function through N17 to regulate trafficking the huntingtin protein between the cytoplasm and nucleus of a cell, and test whether targeting these pathways could prevent the onset or slow the progression of the disease in mouse models of Huntington’s.

The study’s other authors were Jeffrey Cantle, Erin Greiner, C.Y. Daniel Lee, Albert Barth, Fuying Gao, Chang Sin Park, Susanna Sandoval-Miller, Richard Zhang, Istvan Mody and Giovanni Coppola, all of UCLA; and Zhiqiang Zhang and Marc Diamond of the Washington University School of Medicine.

The research was supported by funding from the Hereditary Disease Foundation and the National Institute of Neurological Disorders and Stroke (R01NS049501, R01NS074312, R01NS084298-01). Additional support of the Yang lab’s Huntington’s research is provided by the CHDI Foundation, the McKnight Foundation and the David Weil Fund to the Semel Institute at UCLA.

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Scientists hunt down origin of Huntington’s disease in the brain


UCLA research suggests new targets, routes for drugs to slow the devastating disease.

The gene mutation that causes Huntington’s disease appears in every cell in the body, yet it kills only two types of brain cells. Why? UCLA scientists used a unique approach to switch the gene off in individual brain regions and zero in on those that play a role in causing the disease in mice.

Published in today’s (April 28) online edition of the journal Nature Medicine, the research sheds light on where Huntington’s starts in the brain. It also suggests new targets and routes for therapeutic drugs to slow the devastating disease, which strikes an estimated 35,000 Americans.

“From Day One of conception, the mutant gene that causes Huntington’s appears everywhere in the body, including every cell in the brain,” said X. William Yang, a professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA. “Before we can develop effective strategies to treat the disorder, we need to first identify where it starts and how it ravages the brain.”

Huntington’s disease is passed from parent to child through a mutation in a gene called huntingtin. Scientists blame a genetic “stutter” — a repetitive stretch of DNA at one end of the altered gene — for the cell death and the brain atrophy that progressively deprives patients of their ability to move, speak, eat and think clearly. No cure exists, and people with aggressive cases may die in as little as 10 years.

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Tweaking potassium levels in brain could be a key to fighting Huntington’s


UCLA findings could point to new drug targets for treating the devastating disease.

Astrocytes in brain tissue

By boosting the ability of a specific type of cell to absorb potassium in the brain, UCLA researchers were able to improve walking and prolong survival in a mouse model of Huntington’s disease.

Their findings, published March 30 in the online edition of the journal Nature Neuroscience, could point to new drug targets for treating the devastating disease, which strikes one in every 20,000 Americans.

Huntington’s disease is passed from parent to child through a mutation in the huntingtin gene. By killing brain cells called neurons, the disorder gradually deprives patients of their ability to walk, speak, swallow, breathe and think clearly. No cure exists, and patients with aggressive cases can die in as little as 10 years.

The laboratories of Baljit Khakh, a UCLA professor of physiology and neurobiology, and Michael Sofroniew, a UCLA professor of neurobiology, teamed up at the David Geffen School of Medicine at UCLA to unravel the role that astrocytes — large, star-shaped cells found in the brain and spinal cord — play in Huntington’s.

“Astrocytes appear in the brain in equal numbers to neurons yet haven’t been closely studied,” Khakh said. “They enable neurons to signal each other by maintaining an optimal chemical environment outside the cells. We used two mouse models to explore whether astrocytes behave differently during Huntington’s disease.”

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Single gene mutation linked to neurological disorders


From Lesch-Nyhan syndrome to Alzheimer’s, Parkinson’s and Huntington’s diseases.

Theodore Friedmann, UC San Diego

Theodore Friedmann, UC San Diego

A research team, headed by Theodore Friedmann, M.D., professor of pediatrics at the UC San Diego School of Medicine, says a gene mutation that causes a rare but devastating neurological disorder known as Lesch-Nyhan syndrome appears to offer clues to the developmental and neuronal defects found in other, diverse neurological disorders like Alzheimer’s, Parkinson’s and Huntington’s diseases.

The findings, published in today’s (Oct. 9) issue of the journal PLOS ONE, provide the first experimental picture of how gene expression errors impair the ability of stem cells to produce normal neurons, resulting instead in neurological disease. More broadly, they indicate that at least some distinctly different neurodevelopmental and neurodegenerative disorders share basic, causative defects.

The scientists say that understanding defects in Lesch-Nyhan could help identify errant processes in other, more common neurological disorders, perhaps pointing the way to new kinds of therapies.

Lesch-Nyhan syndrome is caused by defects in the HPRT1 gene (short for hypoxanthine guanine phosphoribosyltransferace, the enzyme it encodes), a gene that is well-known for its essential “housekeeping duties,” among them helping generate purine nucleotides – the building blocks of DNA and RNA.

Mutations in the gene result in deficiencies in the HPRT enzyme, leading to defective expression of the neurotransmitter dopamine and subsequent abnormal neuron function. HPRT mutation is known to be the specific cause of Lesch-Nyhan, an inherited neurodevelopmental disorder characterized by uncontrollable repetitive body movements, cognitive defects and compulsive self-mutilating behaviors. The disorder was first described in 1964 by medical student Michael Lesch and his mentor, William Nyhan, M.D., professor emeritus at UC San Diego School of Medicine.

Using mouse embryonic stem cells modified to be HPRT-deficient, Friedmann and colleagues discovered that the cells do not develop normally. Instead, they differentiate from full-fledged neurons into cells that resemble and partially function as neurons, but also perform functions more typical of glial cells, a kind of supporting cell in the central nervous system. In addition, they noted that HPRT deficiency causes abnormal regulation of many cellular functions controlling important operational and reproduction mechanisms, DNA replication and repair and many metabolic processes.

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Failure to destroy toxic protein contributes to progression of Huntington’s


Study also finds target that boosts protein clearance, prolongs cell life.

Steve Finkbeiner

Steve Finkbeiner

Alzheimer’s, Huntington’s, Parkinson’s.

Names forever linked to what they represent: diseases that ravage the brain’s neurons and leave entire regions to wither and die. These and other so-called neurodegenerative diseases are often associated with the buildup of toxic proteins that lead to neuronal death.

But now, scientists at the Gladstone Institutes have discovered that the progression of disease is not due to the buildup of toxins itself, but rather in the individual neurons’ ability to dissolve them. Further, they have identified a therapeutic target that could boost this ability, thereby protecting the brain from the diseases’ deadly effects.

In the latest issue of Nature Chemical Biology, researchers in the laboratory of Gladstone investigator Steve Finkbeiner, M.D., Ph.D., describe how a newly developed technology allowed them to see – for the first time – how individual neurons fight back against the buildup of toxic proteins over time. Focusing their efforts on a model of Huntington’s disease, the team observed how different types of neurons in the brain each responded to this toxic buildup with different degrees of success, offering clues as to why the disease causes neurons in one region to die, while neurons in another are spared.

“Huntington’s – an inherited and fatal disorder that leads to problems with muscle coordination, cognition and personality – is characterized by the toxic buildup of a mutant form of the huntingtin protein in the brain,” explained Finkbeiner, who directs the Taube-Koret Center for Neurodegenerative Disease Research at Gladstone. Finkbeiner is also a professor of neurology and physiology at UC San Francisco, with which Gladstone is affiliated.

“A long-standing mystery among researchers was how the buildup of this mutant huntingtin caused cells to degrade and die, but previous technology made it virtually impossible to monitor this process at the cellular level,” he added. “In this study, we employed a method called optical pulse-labeling, or OPL, which allowed us to see how the mutant huntingtin ravaged the brain over time – neuron by neuron.”

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UC Irvine studies point to new targets for Huntington’s disease treatments


Studies reveal fundamental mechanism of diseases related to the human brain.

Leslie Thompson, UC Irvine

Leslie Thompson, UC Irvine

UC Irvine MIND’s Leslie Thompson has worked on Huntington’s disease for over two decades, and her group’s research has revealed extensive insights into the biological underpinnings of the disease. Now, her laboratory adds to its impressive log of discoveries.

Thompson is the lead author for studies appearing the week of July 15 in the Proceedings of the National Academy of Sciences and Cell Reports that identify new and well-defined molecular targets for drugs that can treat the fatal neurodegenerative disease.

In the journal Cell Reports, published today (July 18), Thompson and colleagues identify how two proteins – SUMO-2 and PIAS1 – help control the accumulation of the Huntingtin protein in brain tissue. This accumulation is central to disease progression. And in the PNAS article, also published this online week, Thompson and colleagues explore the genetics of HD, reporting that targeting a histone-modifying enzyme (H3K4 demethylase) can normalize the expression of certain aberrant genes that promote disease progression.

“The molecular activities we identified represent defined therapeutic targets,” says Thompson, a professor of psychiatry & human behavior and neurobiology & behavior. “However, they also both reveal fundamental mechanism of diseases related to the human brain, and underscore the importance of basic science research on neurodegenerative diseases.”

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Mapping technique uncovers underlying circuit architecture of the brain


Study to help scientists decode circuitry that guides brain function.

Anatol Kreitzer

The power of the brain lies in its trillions of intercellular connections, called synapses, which together form complex neural “networks.”

While neuroscientists have long sought to map these complex connections to see how they influence specific brain functions, traditional techniques have yet to provide the desired resolution.

Now, by using an innovative brain-tracing technique, scientists at the Gladstone Institutes and the Salk Institute have found a way to untangle these networks. Their findings offer new insight into how specific brain regions connect to each other, while also revealing clues as to what may happen, neuron by neuron, when these connections are disrupted.

In the latest issue of Neuron, a team led by Gladstone investigator Anatol Kreitzer, Ph.D., and Salk investigator Edward Callaway, Ph.D., combined mouse models with a sophisticated tracing technique — known as the monosynaptic rabies virus system — to assemble brain-wide maps of neurons that connect with the basal ganglia, a region of the brain that is involved in movement and decision-making. Developing a better understanding of this region is important as it could inform research into disorders causing basal ganglia dysfunction, including Parkinson’s disease and Huntington’s disease.

“Taming and harnessing the rabies virus – as pioneered by Dr. Callaway – is ingenious in the exquisite precision that it offers compared with previous methods, which were messier with a much lower resolution,” explained Kreitzer, who is also an associate professor of neurology and physiology at UC San Francisco, with which Gladstone is affiliated. “In this paper, we took the approach one step further by activating the tracer genetically, which ensures that it is only turned on in specific neurons in the basal ganglia. This is a huge leap forward technologically, as we can be sure that we’re following only the networks that connect to particular kinds of cells in the basal ganglia.”

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A cause close to her heart


UC Irvine staffer works to end Huntington’s disease.

Frances Saldana, UC Irvine

Frances Saldana, UC Irvine

For two decades, UC Irvine has been on the forefront of Huntington’s disease research and care, and Frances Saldaña is working to keep it that way.

By day, she manages the Corporate Partners program for The Paul Merage School of Business. But Saldaña is better known as a focused and driven advocate for the patients and family members who must endure the terrible consequences of this incurable neurodegenerative disorder.

She shares their pain. Saldaña has lost a husband and her younger daughter to Huntington’s disease, and her other two children are in the late stages of it. “HD is cruel and unfair,” she says. “And we have to end it.”

So along with friends Jean Abdalla and Linda Pimental, who have also lost family members to the disease, Saldaña founded HD CARE to raise awareness and funds for UC Irvine research and clinical care. It’s an official support group of the campus’s Institute for Memory Impairments & Neurological Disorders (UCI MIND), which explores new research and treatments for a spectrum of neurodegenerative diseases, including Alzheimer’s and Parkinson’s.

“Frances is a tireless promoter of HD research and care, and her enthusiasm is infectious,” says Leslie Thompson, a UC Irvine professor of psychiatry & human behavior and neurobiology & behavior who’s recognized as one of the world’s pre-eminent HD researchers. “Her impact is profound.”

Huntington’s disease – a progressive, genetic brain disorder – causes the degeneration of neurons in certain areas of the brain. It’s a familial disease passed from parent to child through a genetic mutation. Symptoms include uncontrolled movements, loss of intellectual capabilities and emotional disturbances. In the U.S. alone, at least 30,000 people have HD, and more than 150,000 others have a 50 percent risk of developing it.

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Regulating single protein prompts fibroblasts to become neurons


Findings could have implications for developing new treatments for Parkinson’s, Alzheimer’s.

Confocal micrograph of a primary human fibroblast cell grown in culture stained blue for actin, a highly abundant protein that makes up the cytoskeleton of cells.Energy-producing mitochondria are shown in green.

Repression of a single protein in ordinary fibroblasts is sufficient to directly convert the cells – abundantly found in connective tissues – into functional neurons. The findings, which could have far-reaching implications for the development of new treatments for neurodegenerative diseases like Huntington’s, Parkinson’s and Alzheimer’s, will be published online in advance of the Jan. 17 issue of the journal Cell.

In recent years, scientists have dramatically advanced the ability to induce pluripotent stem cells to become almost any type of cell, a major step in many diverse therapeutic efforts. The new study focuses upon the surprising and singular role of PTB, an RNA-binding protein long known for its role in the regulation of alternative RNA splicing.

In in vitro experiments, scientists at the UC San Diego School of Medicine and Wuhan University in China describe the protein’s notable regulatory role in a feedback loop that also involves microRNA – a class of small molecules that modulate the expression of up to 60 percent of genes in humans. Approximately 800 miRNAs have been identified and characterized to various degrees.

One of these miRNAs, known as miR-124, specifically modulates levels of PTB during brain development. The researchers found that when diverse cell types were depleted of PTB, they became neuronal-like cells or even functional neurons – an unexpected effect. The protein, they determined, functions in a complicated loop that involves a group of transcription factors dubbed REST that silences the expression of neuronal genes in non-neuronal cells.

According to principal investigator Xiang-Dong Fu, Ph.D., professor of cellular and molecular medicine at UC San Diego, it’s not known which neuronal signal or signals turn on the loop, which in principle can happen at any point in the circle. But the ability to artificially manipulate PTB levels in cells, inducing them to become neurons, offers tantalizing possibilities for scientists seeking new treatments for an array of neurodegenerative diseases.

It is estimated that over a lifetime, 1 in 4 Americans will suffer from a neurodegenerative disease, from Alzheimer’s and Parkinson’s to multiple sclerosis and amyotrophic lateral sclerosis (Lou Gehrig’s disease).

“All of these diseases are currently incurable. Existing therapies focus on simply trying to preserve neurons or slow the rate of degeneration,” said Fu. “People are working with the idea of replacing lost neurons using embryonic stem cells, but there are a lot of challenges, including issues like the use of foreign DNA and the fact that it’s a very complex process with low efficiency.”

Fu explained that REST is expressed in cells everywhere except in neurons. PTB is itself a target of miR-124, but also acts as a break for this microRNA to attack other cellular targets that include REST, which is responsible for repressing miR-124.

In non-neuronal cells, REST keeps miR-124 down and PTB enforces this negative feedback loop, but during neural induction, miR-124 is induced, which diminishes PTB, and without PTB as a break, REST is dismantled, and without REST, additional miR-124 is produced. This loop therefore becomes a positive feed forward, which turns non-neuronal cells into neurons.

“If we learn how to manipulate PTB, which appears to be a kind of master regulator, we might eventually be able to avoid some of these problems by creating new neurons in patients using their own cells adjacent deteriorating neurons,” said Fu.

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Berkeley Lab scientists help develop promising therapy for Huntington’s


Initial results in mice could lead to new way to fight neurodegenerative diseases.

Mitochondria are labeled red and green, and the nucleus is blue, in this neuron isolated from a Huntington's disease mouse model.

There’s new hope in the fight against Huntington’s disease. A group of researchers that includes scientists from the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) have designed a compound that suppresses symptoms of the devastating disease in mice.

The compound is a synthetic antioxidant that targets mitochondria, an organelle within cells that serves as a cell’s power plant. Oxidative damage to mitochondria is implicated in many neurodegenerative diseases including Alzheimer’s, Parkinson’s and Huntington’s.

The scientists administered the synthetic antioxidant, called XJB-5-131, to mice that have a genetic mutation that triggers Huntington’s disease. The compound improved mitochondrial function and enhanced the survival of neurons. It also inhibited weight loss and stopped the decline of motor skills, among other benefits. In short, the Huntington’s mice looked and behaved like normal mice.

Based on their findings, the scientists believe that XJB-5-131 is a promising therapeutic compound that deserves further investigation as a way to fight neurodegenerative diseases.

They report their research in a paper that appears online Nov. 1 in the journal Cell Reports.

“The compound was very successful. More research is needed, but it has the real potential to make an impact in treating neurodegenerative disorders,” says Cynthia McMurray of Berkeley Lab’s Life Sciences Division. She conducted the research with other Berkeley Lab researchers, including Zhiyin Xun, and scientists from the University of Pittsburgh.

Huntington’s disease is a genetic disorder in which neurons in certain parts of the brain waste away. Symptoms of the disease typically appear in mid-life. These include loss of muscle coordination and cognitive decline. There is no cure. Currently, patients are prescribed antidepressants or compounds that reduce the loss of motor coordination, neither of which delays the disease’s progression.

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