Friday, January 18, 2019

Does the ketogenic diet really improve brain function

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University of Kentucky - UK HealthCare

In the lab, the Ketogenic Diet increased cerebral blood flow, improved the gut microbiome, lowered glucose as well as weight, and boosted the brain's process that clears Alzheimer's amyloid-beta plaque. Learn more. 




LEXINGTON, Ky. — Ai-Ling Lin, and her colleagues at the University of Kentucky Sanders-Brown Center on Aging, have published an important study demonstrating the effects of the Ketogenic Diet on cognitive health in the lab. 

Published in Scientific Reports, the study demonstrated that neurovascular function improved in mice who followed a Ketogenic Diet regimen. 


Diet Enhances Neurovascular Integrity

"Neurovascular integrity, including cerebral blood flow and blood-brain barrier function, plays a major role in cognitive ability," Lin said. "Recent science has suggested that neurovascular integrity might be regulated by the bacteria in the gut, so we set out to see whether the Ketogenic Diet enhanced brain vascular function and reduced neurodegeneration risk in young healthy mice." 

Lin et al considered The Ketogenic Diet — characterized by high levels of fat and low levels of carbohydrates — a good candidate for the study, as it has previously shown positive effects for patients with other neurological disorders, including epilepsy, Parkinson's disease, and autism.

Ketogenic Diet or Regular Diet?

Two groups of nine mice, aged 12-14 weeks, were given either the Ketogenic Diet (KD) or a regular diet. After 16 weeks, Lin et al saw that the KD mice had significant increases in cerebral blood flow, improved balance in the microbiome in the gut, lower blood glucose levels and body weight, and a beneficial increase in the process that clears amyloid-beta from the brain — a hallmark of Alzheimer's disease. 

"While diet modifications, the Ketogenic Diet in particular, has demonstrated effectiveness in treating certain diseases, we chose to test healthy young mice using diet as a potential preventative measure," Lin said. "We were delighted to see that we might indeed be able to use diet to mitigate risk for Alzheimer's disease." 

According to Lin, the beneficial effects seen from the Ketogenic Diet are potentially due to the inhibition of a nutrient sensor called mTOR (mechanistic target of rapamycin), which has shown to affect lifespan extension and health promotion. In addition to the Ketogenic Diet, Lin said, mTOR can also be inhibited by simple caloric restriction. 


Wednesday, January 16, 2019

5 million dollars Who will find Alzheimer's cause?

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The University of Texas at San Antonio

The world’s largest prize of its kind is challenging researchers to find the cause of Alzheimer's. Set by James Truchard, the retired CEO of corporate giant National Instruments, learn how this contest will bring together the world’s best minds to consider the entire Alzheimer's puzzle. 




SAN ANTONIO--(BUSINESS WIRE)--To expand the understanding and explanation of Alzheimer’s disease, United States businessman James Truchard has given a $5 million USD gift to The University of Texas at San Antonio (UTSA) College of Sciences to establish the Oskar Fischer Project. The initiative will engage the world’s brightest minds in a comprehensive literature review with the goal of synthesizing that information into one simple explanation for the cause of Alzheimer’s disease. The challenge was announced during the Society for Neuroscience’s annual meeting, an international gathering of nearly 30,000 scientists in the United States. 

World's Largest Prizes

Truchard, retired president and chief executive officer of United States-based technology company National Instruments, conceptualized and established the Oskar Fischer Project to engage the world’s brightest minds. The challenge will award up to $4 million USD in Oskar Fischer Prizes, including a grand prize of $2 million, two second place prizes of $500,000 each and four third place prizes of $250,000 each. Collectively, the monetary awards are the world’s largest prizes of their kind. 

Through personal research, Truchard, 75, was introduced to the work of Oskar Fischer (1876-1942), a Jewish pioneer in neuroscience who studied dementia at the same time as Alois Alzheimer. In 1900, Fischer began working at Charles University’s German University, based in Prague. His research led to the identification of senile plaques (then called neuritic plaques), the signature lesions of Alzheimer’s disease. 

Fischer hypothesized that the plaques were associated with presbyophrenia, then characterized as a form of senile dementia marked by memory loss, memory distortions and disorientation. He published on 12 patients with plaques and tangles, protein strands that appear during Alzheimer’s disease, in 1907, the same year that Alzheimer published on one patient with early onset Alzheimer’s. 

Fischer remained at the German University until he was removed in 1939. Two years later, he was sent to Theresienstadt in TerezĂ­n, a way station for Auschwitz and Treblinka. He died in 1942, unable to survive the harsh conditions of the concentration camp.

Solve the Alzheimer's Puzzle

“A century has passed since Oskar Fischer’s seminal work, and tens of billions have been spent around the world on research and potential cures. Over 130,000 research papers have been published and yet no definitive explanation and cure for Alzheimer’s has been found,” said Truchard. “We need to look at Alzheimer’s as a big complex puzzle with a missing piece. We need a brilliant individual who can take all of the pieces and consider what each offers, and then develop one explanation that fits because it pulls all of the pieces together and makes the puzzle whole.” 

According to the World Alzheimer Report 2018 by Alzheimer’s Disease International (ADI), an estimated 50 million people worldwide are living with dementia at a cost of $1 trillion to the global economy. That population is expected to more than triple by the year 2050, according to ADI, which also reports that the global ratio of publications on neurodegenerative disorders versus cancer is just one to 12. 

“The Oskar Fischer Project will take a new systems approach to the research on Alzheimer’s, building on the work Oskar Fischer started over a century ago,” said George Perry, chief scientist of the UTSA Brain Health Consortium. “Jim Truchard’s generous gift will create an international forum to assess that work and bring forward an explanation that will advance society’s understanding of the disease.” 

The University of Texas at San Antonio, a world leader in brain health research, will incubate the two-year challenge. In the UTSA Brain Health Consortium, 38 of the nation’s brightest scientists are engaged in research on brain mechanisms and therapeutics. The university’s researchers have expertise in neurodegenerative disease, brain circuits and electrical signaling, traumatic brain injury, regenerative medicine and stem cell therapies, medicinal chemistry and drug design, neuroinflammation, and psychology.

Unraveling the Mysteries of Neurodegeneration

“Through Jim Truchard’s support, the Oskar Fischer Project will accelerate our shared mission of unraveling the mysteries of neurodegeneration through engagement with the smartest thinkers around the world,” said UTSA President Taylor Eighmy. 

Truchard added, “I truly believe that Alzheimer’s disease is multifaceted; it’s about lifestyle, heredity and brain regression. It’s important to look at all possible solutions. This contest will bring together the world’s best minds to consider the entire story.” 

UTSA will work closely with an interdisciplinary committee of outstanding scientists from Texas to award the Oskar Fischer Prizes. The call for proposals will open in February 2019 and will continue through the two-year term of the project. 


SOURCE:

  • The University of Texas at San Antonio
    The University of Texas at San Antonio (UTSA) is a public urban serving university specializing in health, cybersecurity, energy, sustainability, and human and social development. With more than 32,000 students, it is the largest university in the San Antonio metropolitan region. UTSA advances knowledge through research and discovery, teaching and learning, community engagement and public service. The university embraces multicultural traditions and serves as a center for intellectual and creative resources as well as a catalyst for socioeconomic development and the commercialization of
    intellectual property—for Texas, the nation and the world

Monday, January 14, 2019

How to slow the accumulation of brain plaque

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 American Chemical Society

Beets get red from betanin. Betanin slows the accumulation of brain plaque, Alzheimer's #1 culprit. Learn how. See NutritionFacts.org's Dr. Greger on the way fresh beets fight dementia, and how much to eat or drink. 




"Our data suggest that betanin, a compound in beet extract, shows some promise as an inhibitor of certain chemical reactions in the brain that are involved in the progression of Alzheimer's disease," says Li-June Ming, Ph.D. "This is just a first step, but we hope that our findings will encourage other scientists to look for structures similar to betanin that could be used to synthesize drugs that could make life a bit easier for those who suffer from this disease." 

Saturday, January 12, 2019

Benefits of turmeric

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Salk Institute's J147 is a derivative of turmeric, a spice used in curry. Learn how it fights memory deficits and has a host of unexpected anti-aging effects in the lab. 




Salk Institute researchers have found that J147, which is an experimental drug candidate aimed at combating Alzheimer's disease, has a host of unexpected anti-aging effects in animals.

J147, Alzheimer's and Old Age

The Salk team expanded upon their previous development of the drug candidate they labeled J147. It is a derivative of the common spice, turmeric, and takes a different tack by targeting Alzheimer's major risk factor -- old age. In the new work, the team showed that the drug candidate worked well in a mouse model of aging not typically used in Alzheimer's research. When these mice were treated with J147, they had better memory and cognition, healthier blood vessels in the brain and other improved physiological features, as detailed in the journal Aging.

Fighting Alzheimer's By Fighting Aging

"Initially, the impetus was to test this drug in a novel animal model that was more similar to 99 percent of Alzheimer's cases," says Antonio Currais, the lead author and a member of Professor David Schubert's Cellular Neurobiology Laboratory at Salk. "We did not predict we'd see this sort of anti-aging effect, but J147 made old mice look like they were young, based upon a number of physiological parameters."

Alzheimer's disease is a progressive brain disorder, recently ranked as the third leading cause of death in the United States and affecting more than five million Americans. It is also the most common cause of dementia in older adults, according to the National Institutes of Health.

"While most drugs developed in the past 20 years target the amyloid plaque deposits in the brain (which are a hallmark of the disease), none have proven effective in the clinic," says Schubert, senior author of the study.

Expanding the Fight to More Common Dementias

Several years ago, Schubert and his colleagues began to approach the treatment of the disease from a new angle. Rather than target amyloid, the lab decided to zero in on the major risk factor for the disease--old age. Using cell-based screens against old age-associated brain toxicities, they synthesized J147.

Previously, the team found that J147 could prevent and even reverse memory loss and Alzheimer's pathology in mice that have a version of the inherited form of Alzheimer's, the most commonly used mouse model. However, this form of the disease comprises only about 1 percent of Alzheimer's cases. For everyone else, old age is the primary risk factor, says Schubert. The team wanted to explore the effects of the drug candidate on a breed of mice that age rapidly and experience a version of dementia that more closely resembles the age-related human disorder.

Young Mice, Old Mice and J147-fed Mice

In this latest work, the researchers used a comprehensive set of assays to measure the expression of all genes in the brain, as well as over 500 small molecules involved with metabolism in the brains and blood of three groups of the rapidly aging mice. The three groups of rapidly aging mice included one set that was young, one set that was old and one set that was old but fed J147 as they aged.

7 Benefits

The old mice fed J147 saw the following benefits:
  1. They performed better on memory and other tests for cognition
  2. They displayed more robust motor movements.
  3. They had fewer pathological signs of Alzheimer's in their brains.
  4. J147 prevented the leakage of blood from the microvessels in the brains of old mice. "Damaged blood vessels are a common feature of aging in general, and in Alzheimer's, it is frequently much worse," says Currais.

    Importantly, because of the large amount of data collected on the three groups of mice, it was possible to demonstrate that many aspects of gene expression and metabolism in the old mice fed J147 were very similar to those of the young animals. These included:
  5. markers for increased energy metabolism,
  6. reduced brain inflammation and
  7. reduced levels of oxidized fatty acids in the brain.

Human Clinical Trials

Currais and Schubert note that while these studies represent a new and exciting approach to Alzheimer's drug discovery and animal testing in the context of aging, the only way to demonstrate the clinical relevance of the work is to move J147 into human clinical trials for Alzheimer's disease.

"If proven safe and effective for Alzheimer's, the apparent anti-aging effect of J147 would be a welcome benefit," adds Schubert. The team aims to begin human trials next year.

Related Article:

Curry Derivative J147 Beats Aricept for Alzheimer's


MORE INFORMATION:
  • Other authors on the paper include Oswald Quehenberger of the University of California, San Diego; and Joshua Goldberg, Catherine Farrokhi, Max Chang, Marguerite Prior, Richard Dargusch, Daniel Daugherty and Pamela Maher of the Salk Institute.
  • This study was supported by the Salk Institute Pioneer Fund Postdoctoral Scholar Award and the Salk Nomis Fellowship Award, fellowships from the Hewitt Foundation and Bundy Foundation, and grants from the Burns Foundation and NIH.
SOURCE:

Thursday, January 10, 2019

Alzheimer's-Where why and how

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Columbia University Medical Center, via Newswise.

3 ROOTS OF ALZHEIMER'S: 

Columbia University researchers have pinpointed 3 discoveries about Alzheimer's:

  • Where it starts
  • Why it starts there
  • How it spreads.
Learn why this can help researchers treat Alzheimer's sooner and better

discoveries about Alzheimer's:
  • Where it starts
  • Why it starts there
  • How it spreads.
Learn why this can help researchers treat Alzheimer's sooner and better. 




Using high-resolution functional MRI (fMRI) imaging in patients with Alzheimer's disease and in mouse models of the disease, Columbia University Medical Center (CUMC) researchers have clarified three fundamental issues about Alzheimer's: where it starts, why it starts there, and how it spreads. In addition to advancing understanding of Alzheimer's, the findings could improve early detection of the disease, when drugs may be most effective. The study was published today in the online edition of the journalNature Neuroscience.



Alzheimer's disease starts in the entorhinal cortex (yellow). Using fMRI in mouse (left) and human (right) brains, the researchers provide evidence that the disease spreads from the entohrinal cortex (yellow) to other cortical regions (red) -- the perirhinal cortex and posterior parietal cortex. (Credit: Usman Khan/lab of Scott A. Small, MD, Columbia University Medical Center.)

"It has been known for years that Alzheimer's starts in a brain region known as the entorhinal cortex," said co-senior author Scott A. Small, MD, Boris and Rose Katz Professor of Neurology, professor of radiology, and director of the Alzheimer's Disease Research Center. "But this study is the first to show in living patients that it begins specifically in the lateral entorhinal cortex, or LEC. The LEC is considered to be a gateway to the hippocampus, which plays a key role in the consolidation of long-term memory, among other functions. If the LEC is affected, other aspects of the hippocampus will also be affected."

The study also shows that, over time, Alzheimer's spreads from the LEC directly to other areas of the cerebral cortex, in particular, the parietal cortex, a brain region involved in various functions, including spatial orientation and navigation. The researchers suspect that Alzheimer's spreads "functionally," that is, by compromising the function of neurons in the LEC, which then compromises the integrity of neurons in adjoining areas.

A third major finding of the study is that LEC dysfunction occurs when changes in tau and amyloid precursor protein (APP) co-exist. "The LEC is especially vulnerable to Alzheimer's because it normally accumulates tau, which sensitizes the LEC to the accumulation of APP. Together, these two proteins damage neurons in the LEC, setting the stage for Alzheimer's," said co-senior author Karen E. Duff, PhD, professor of pathology and cell biology (in psychiatry and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute.

In the study, the researchers used a high-resolution variant of fMRI to map metabolic defects in the brains of 96 adults enrolled in the Washington Heights-Inwood Columbia Aging Project (WHICAP). All of the adults were free of dementia at the time of enrollment.

"Dr. Richard Mayeux's WHICAP study enables us to follow a large group of healthy elderly individuals, some of whom have gone on to develop Alzheimer's disease," said Dr. Small. "This study has given us a unique opportunity to image and characterize patients with Alzheimer's in its earliest, preclinical stage."

The 96 adults were followed for an average of 3.5 years, at which time 12 individuals were found to have progressed to mild Alzheimer's disease. An analysis of the baseline fMRI images of those 12 individuals found significant decreases in cerebral blood volume (CBV) -- a measure of metabolic activity -- in the LEC compared with that of the 84 adults who were free of dementia.

A second part of the study addressed the role of tau and APP in LEC dysfunction. While previous studies have suggested that entorhinal cortex dysfunction is associated with both tau and APP abnormalities, it was not known how these proteins interact to drive this dysfunction, particularly in preclinical Alzheimer's.

To answer this question, explained first author Usman Khan, an MD-PhD student based in Dr. Small's lab, the team created three mouse models, one with elevated levels of tau in the LEC, one with elevated levels of APP, and one with elevated levels of both proteins. The researchers found that the LEC dysfunction occurred only in the mice with both tau and APP.

The study has implications for both research and treatment. "Now that we've pinpointed where Alzheimer's starts, and shown that those changes are observable using fMRI, we may be able to detect Alzheimer's at its earliest preclinical stage, when the disease might be more treatable and before it spreads to other brain regions," said Dr. Small. In addition, say the researchers, the new imaging method could be used to assess the efficacy of promising Alzheimer's drugs during the disease's early stages.


The paper is titled, "Molecular drivers and cortical spread of lateral entorhinal cortex dysfunction in preclinical Alzheimer's disease." The other contributors are Li Liu, Frank Provenzano, Diego Berman, Caterina Profaci, Richard Sloan and Richard Mayeux, all at CUMC.

The study was supported by grants from National Institutes of Health (AG034618, AG025161, AG07232, AG037212, NS074874, and HL094423.

Source:

Columbia University Medical Center, via Newswise.

Journal Reference:
  1. Usman A Khan, Li Liu, Frank A Provenzano, Diego E Berman, Caterina P Profaci, Richard Sloan, Richard Mayeux, Karen E Duff, Scott A Small. Molecular drivers and cortical spread of lateral entorhinal cortex dysfunction in preclinical Alzheimer's diseaseNature Neuroscience, 2013; DOI: 10.1038/nn.3606

Tuesday, January 8, 2019

Alzheimer's-Best ways to deal with incontinence

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

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The Dementia Caregiver's Little Book of Hope [Kindle Edition]

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Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two

The Alzheimer's Disease Education and Referral (ADEAR) Center 


Here are some good ways you can deal with incontinence in dementia care. 




A person with Alzheimer’s disease may have other medical problems over time. These problems can cause more confusion and behavior changes. The person may not be able to tell you what is wrong.

One problem, incontinence, means a person can’t control his or her bladder and/or bowels. This may happen at any stage of Alzheimer’s disease, but it is more often a problem in the later stages. Signs of this problem are leaking urine, problems emptying the bladder, and soiled underwear and bed sheets. Let the doctor know if you see any of these signs. He or she may be able to treat the cause of the problem.

Causes of Incontinence

  1. Incontinence has several possible causes. Some can be treated:
  2. Urinary tract infection
  3. Enlarged prostate gland
  4. Too little fluid in the body (dehydration)
  5. Diabetes that isn’t being treated
  6. Taking too many water pills
  7. Drinking too much caffeine
  8. Taking medicines that make it hard to hold urine
When you talk to the doctor, be ready to answer the following questions:
  • What medicines is the person with Alzheimer’s taking?
  • Does the person leak urine when he or she laughs, coughs, or lifts something?
  • Does the person urinate often?
  • Can the person get to the bathroom in time?
  • Is the person urinating in places other than the bathroom?
  • Is the person soiling his or her clothes or bed sheets each night?
  • Do these problems happen each day or once in a while?

What To Do About Incontinence

Here are some ways you can deal with incontinence:
  1. Remind the person to go to the bathroom every 2 to 3 hours. Don’t wait for him or her to ask.
  2. Show the person the way to the bathroom, or take him or her.
  3. Watch for signs that the person may have to go to the bathroom, such as restlessness or pulling at clothes. Respond quickly.
  4. Make sure that the person wears loose, comfortable clothing that is easy to remove.
  5. Limit fluids after 6 p.m. if problems happen at night. Do not give the person fluids with caffeine, such as coffee or tea.
  6. Give the person fresh fruit before bedtime instead of fluids if he or she is thirsty.
Here are some other tips:
  • Mark the bathroom door with a big sign that reads “Toilet” or “Bathroom.”
  • Use a stable toilet seat that is at a good height. Using a colorful toilet seat may help the person identify the toilet. You can buy raised toilet seats at medical supply stores.
  • Plan ahead if you are going out with the person. Know where restrooms are located. Take an extra set of clothing in case of an accident.
  • Help the person when he or she needs to use a public bathroom. This may mean going into the stall with the person or using a family or private bathroom.

Accidents Happen

Be understanding when bathroom accidents occur. Stay calm and reassure the person if he or she is upset. 

Incontinence supplies, such as adult disposable briefs or underwear, bed protectors, and waterproof mattress covers, may be helpful. You can buy these items at drugstores and medical supply stores. A drainable pouch may be useful for the person who can’t control his or her bowel movements. Talk to a nurse about how to use this product. 

Some people find it helpful to keep a record of how much food and fluid the person with Alzheimer’s takes in and how often he or she goes to the bathroom. You can use this information to make a schedule for going to the bathroom. 


MORE INFORMATION:
SOURCE:
The Alzheimer's Disease Education and Referral (ADEAR) Center 

Sunday, January 6, 2019

CRISPR genetic editing takes another big step forward, targeting RNA

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 an easyceu or two

Salk scientists create new molecular scissors to correct protein imbalance in cellular model of dementia

LA JOLLA—Most people have heard of the CRISPR/Cas9 gene-editing technology, which acts as targeted molecular scissors to cut and replace disease-causing genes with healthy ones. But DNA is only part of the story; many genetic diseases are caused by problems with RNA, a working copy of DNA that is translated into proteins.


Now, Salk Institute scientists have created a new tool that targets not DNA, but RNA, and used it to correct a protein imbalance in cells from a dementia patient, restoring them to healthy levels. The new Salk tool, called CasRx, opens up the vast potential of RNA and proteins to genetic engineering, giving researchers a powerful way to develop new gene therapies as well as investigate fundamental biological functions. The work appeared in Cell on March 15, 2018.
“Bioengineers are like nature’s detectives, searching for clues in patterns of DNA to help solve the mysteries of genetic diseases,” says Patrick Hsu, a Helmsley-Salk Fellow and senior author of the new paper. “CRISPR has revolutionized genome engineering, and we wanted to expand the toolbox from DNA to RNA.”



CRISPRs are bacterial immune systems that contain many defense enzymes such as the Cas9 “molecular scissors,” which scientists including Hsu have engineered as a powerful DNA-targeting gene-editing tool.
The Salk team decided to search bacterial genomes for new CRISPR enzymes that could target RNA, which could then be engineered to address problems with RNA and resulting proteins.
A given RNA message, for example, can be expressed at varying levels and its balance relative to other RNAs is critical for healthy function. Furthermore, RNA can be spliced in various ways to make different proteins, but problems with splicing can lead to diseases such as spinal muscular atrophy, atypical cystic fibrosis and frontotemporal dementia (FTD). So a drug that targets toxic RNAs or RNAs resulting from improper splicing could have a life-changing impact for people with these types of devastating diseases.
“We began the project with the hypothesis that different CRISPR systems may have been specialized throughout an evolutionary arms race between bacteria and their viruses, potentially giving them the ability to target viral RNA,” explains Salk Research Associate Silvana Konermann, an HHMI Hanna Gray Fellow and the paper’s first author.
The team developed a computational program to search bacterial DNA databases for the telltale signatures of CRISPR systems: patterns of particular repeating DNA sequences. In doing so, they discovered a family of CRISPR enzymes that targets RNA, and called it Cas13d.
The team realized that, just like the Cas9 family, Cas13d enzymes originating from different bacterial species would vary in their activity, so they ran a screen to identify the best version for use in human cells. That version turned out to be from the gut bacterium Ruminococcus flavefaciens XPD3002, which led them to name their tool CasRx.
“Once we engineered CasRx to work well in human cells, we really wanted to put it through its paces,”
says Konermann.image.
That meant engineering CasRx to tackle a disease-related condition: in this case, the neurodegenerative disorder FTD. In this dementia, the ratio of two versions of the tau protein (also implicated in Alzheimer’s disease) is out of balance in neurons. The team genetically engineered CasRx to target RNA sequences for the version of the tau protein that is overabundant. They did this by packaging CasRx into a virus and delivering it to neurons grown from an FTD patient’s stem cells. CasRx was 80 percent effective in rebalancing the levels of tau protein to healthy levels.
Compared to other technologies that target RNA, CasRx is unique due to its small size (making it easier to package into therapeutically relevant viral vectors), its high degree of effectiveness, and the fact that it created no discernible off-target effects compared to RNA interference. The Salk team is excited about the possibilities their tool opens up for exploring new biological questions about RNA and protein function, as well as therapies to tackle RNA and protein-based diseases.
“Nature is full of so many secrets,” adds Hsu. “It’s really a rich, untapped resource for inventing new technologies.”
Other authors included Peter Lotfy, Nicholas J. Brideau, Jennifer Oki and Maxim N. Shokhirev, all at the Salk Institute.

The work and researchers involved were supported by an NIH Director’s Early Independence Award, the National Institutes on Aging, the Helmsley Charitable Trust, a Catharina Foundation Fellowship, a Howard Hughes Medical Institute Hanna H. Gray Fellowship, and the Salk Women & Science Special Award.

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