New water batteries stay cool under pressure

 A global team of researchers and industry collaborators led by RMIT University has invented recyclable 'water batteries' that won't catch fire or explode.

Lithium-ion energy storage dominates the market due to its technological maturity, but its suitability for large-scale grid energy storage is limited by safety concerns with the volatile materials inside.

Lead researcher Distinguished Professor Tianyi Ma said their batteries were at the cutting edge of an emerging field of aqueous energy storage devices, with breakthroughs that significantly improve the technology's performance and lifespan.

"What we design and manufacture are called aqueous metal-ion batteries -- or we can call them water batteries," said Ma, from RMIT's School of Science.

The team use water to replace organic electrolytes -- which enable the flow of electric current between the positive and negative terminals -- meaning their batteries can't start a fire or blow up -- unlike their lithium-ion counterparts.

"Addressing end-of-life disposal challenges that consumers, industry and governments globally face with current energy storage technology, our batteries can be safely disassembled and the materials can be reused or recycled," Ma said.

The simplicity of manufacturing processes for their water batteries helped make mass production feasible, he said.

"We use materials such as magnesium and zinc that are abundant in nature, inexpensive and less toxic than alternatives used in other kinds of batteries, which helps to lower manufacturing costs and reduces risks to human health and the environment."

What's the energy-storage and life-cycle potential?

The team has made a series of small-scale trial batteries for numerous peer-reviewed studies to tackle various technological challenges, including boosting energy storage capacity and the lifespan.

In their latest work, published in Advanced Materials, they've triumphed over a major challenge -- the growth of disruptive dendrites, which are spiky metallic formations that can lead to short circuits and other serious faults.

The team coated affected battery parts with a metal called bismuth and its oxide (otherwise known as rust) as a protective layer that prevented dendrite formation.

The result?

"Our batteries now last significantly longer -- comparable to the commercial lithium-ion batteries in the market -- making them ideal for high-speed and intensive use in real-world applications.

"With impressive capacity and extended lifespan, we've not only advanced battery technology but also successfully integrated our design with solar panels, showcasing efficient and stable renewable energy storage."

Source: Sciencedaily

Cleaning or desalinating water quickly: Looking deep into smallest pores

 Membranes of vertically aligned carbon nanotubes (VaCNT) can be used to clean or desalinate water at high flow rate and low pressure. Recently, researchers of Karlsruhe Institute of Technology (KIT) and partners carried out steroid hormone adsorption experiments to study the interplay of forces in the small pores. They found that VaCNT of specific pore geometry and pore surface structure are suited for use as highly selective membranes. The researchers report in Nature Communications.

Clean drinking water is of vital importance to all people worldwide.

Membranes are used to efficiently remove micropollutants, such as steroid hormones that are harmful to health and the environment.

A very promising membrane material is made of vertically aligned carbon nanotubes (VaCNT). "This material is amazing -- with small pores of 1.7 to 3.3 nanometers in diameter, a nearly perfect cylindrical shape, and small torsion," says Professor Andrea Iris Schäfer, who heads KIT's Institute for Advanced Membrane Technology (IAMT). "The nanotubes should have a highly adsorbing effect, but have a very low friction only." Currently, pores are too large for effective retention, but smaller pores are not yet feasible technically.

Interplay of Forces

In experiments with steroid micropollutants, IAMT researchers studied why VaCNT membranes are perfect water filters.

They used membranes produced by the Lawrence Livermore National Laboratory (LLNL) in Livermore (California, USA). The finding: The low adsorption of VaCNT, i.e. deposition on the surface, is desirable for highly selective membranes targeting special substances.

The study reveals that adsorption in membrane nanopores does not only depend on the adsorption surface and the limited mass transfer, but also on the interplay of hydrodynamic forces, friction, and the forces of attraction and repulsion at the liquid-wall interface.

Highly water-permeable nanopores exhibit low interaction due to the small friction and the high flow rate.

"When the molecules are not retained because of their size, interaction with the material will often determine what happens. The molecules will bounce through the membrane similar to a climber climbing a wall. This is much easier when there are many good climbing holds," Schäfer explains.

Studies like that performed by IAMT help to specifically design pore geometry and pore surface structure.

Ten Years to Turn the Idea into an Experiment

The membranes were developed by Dr. Francesco Fornasiero and his team at LLNL.

The experiments with the micropollutants were carried out and evaluated using latest analytical instruments at IAMT.

"It took about ten years to turn the idea into a successful experiment that has met with the wide interest of the membrane technology community," Schäfer says.

Production of such nearly perfect membranes is extremely difficult.

Source: ScienceDaily

Revealing what makes bacteria life-threatening

 Queensland researchers have discovered that a mutation allows some E. coli bacteria to cause severe disease in people while other bacteria are harmless, a finding that could help to combat antibiotic resistance.

Professor Mark Schembri and Dr Nhu Nguyen from The University of Queensland's Institute for Molecular Bioscience and Associate Professor Sumaira Hasnain from Mater Research found the mutation in the cellulose making machinery of E. coli bacteria.

Professor Schembri said the mutation gives the affected E. coli bacteria the green light to spread further into the body and infect more organs, such as the liver, spleen and brain.

"Our discovery explains why some E. coli bacteria can cause life-threatening sepsis, neonatal meningitis and urinary tract infections (UTIs), while other E. coli bacteria can live in our bodies without causing harm," Professor Schembri said.

"The 'good' bacteria make cellulose and 'bad' bacteria can't."

Bacteria produce many substances on their cell surfaces that can stimulate or dampen the immune system of the host.

"The mutations we identified stopped the E. coli making the cell-surface carbohydrate cellulose and this led to increased inflammation in the intestinal tract of the host," Professor Schembri said.

"The result was a breakdown of the intestinal barrier, so the bacteria could spread through the body."

In models that replicate human disease, the team showed that the inability to produce cellulose made the bacteria more virulent, so it caused more severe disease, including infection of the brain in meningitis and the bladder in UTIs.

Associate Professor Hasnain said understanding how bacteria spread from intestinal reservoirs to the rest of the body was important in preventing infections.

"Our finding helps explain why certain types of E. coli become more dangerous and provides an explanation for the emergence of different types of highly virulent and invasive bacteria," she said.

Professor Schembri said E. coli was the most dominant pathogen associated with bacterial antibiotic resistance.

"In 2019 alone, almost 5 million deaths worldwide were associated with bacterial antibiotic resistance, with E. coli causing more than 800,000 of these deaths," he said.

"As the threat of superbugs that are resistant to all available antibiotics increases worldwide, finding new ways to prevent this infection pathway is critical to reduce the number of human infections."

The collaboration included teams from UQ's School of Biomedical Sciences led by Associate Professor Jana Vukovic and from Griffith University's School of Pharmacy and Medical Sciences led by Professor Glen Ulett.

Source: ScienceDaily

Science fiction meets reality: New technique to overcome obstructed views

 After a recent car crash, John Murray-Bruce wished he could have seen the other car coming. The crash reaffirmed the University of South Florida assistant professor of computer science and engineering's mission to create a technology that could do just that: See around obstacles and ultimately expand one's line of vision.

Using a single photograph, Murray-Bruce and his doctoral student, Robinson Czajkowski, created an algorithm that computes highly accurate, full-color three-dimensional reconstructions of areas behind obstacles -- a concept that can not only help prevent car crashes, but help law enforcement experts in hostage situations, search-and-rescue and strategic military efforts.

"We're turning ordinary surfaces into mirrors to reveal regions, objects and rooms that are outside our line of vision," Murray-Bruce said.

"We live in a 3D world, so obtaining a more complete 3D picture of a scenario can be critical in a number of situations and applications."

As published in Nature Communications, Czajkowski and Murray-Bruce's research is the first-of-its-kind to successfully reconstruct a hidden scene in 3D using an ordinary digital camera.

The algorithm works by using information from the photo of faint shadows cast on nearby surfaces to create a high-quality reconstruction of the scene.

While it is more technical for the average person, it could have broad applications.

"These shadows are all around us," Czajkowski said. "The fact we can't see them with our naked eye doesn't mean they're not there."

The idea of seeing around obstacles has been a topic of science-fiction movies and books for decades.

Murray-Bruce says this research takes significant strides in bringing that concept to life.

Prior to this work, researchers have only used ordinary cameras to create rough 2D reconstructions of small spaces.

The most successful demonstrations of 3D imaging of hidden scene all required specialized, expensive equipment.

"Our work achieves a similar result using far less," Czajkowski said.

"You don't need to spend a million dollars on equipment for this anymore."

Czajkowski and Murray-Bruce expect it will be 10 to 20 years before the technology is robust enough to be adopted by law enforcement and car manufacturers.

Right now, they plan to continue their research to further improve the technology's speed and accuracy to expand its applications in the future, including self-driving cars to improve their safety and situational awareness.

"In just over a decade since the idea of seeing around corners emerged, there has been remarkable progress and there is accelerating interest and research activity in the area," Murray-Bruce said.

Source: ScienceDaily

Brightest and fastest-growing: Astronomers identify record-breaking quasar

 Using the European Southern Observatory's (ESO) Very Large Telescope (VLT), astronomers have characterised a bright quasar, finding it to be not only the brightest of its kind, but also the most luminous object ever observed. Quasars are the bright cores of distant galaxies and they are powered by supermassive black holes. The black hole in this record-breaking quasar is growing in mass by the equivalent of one Sun per day, making it the fastest-growing black hole to date.

The black holes powering quasars collect matter from their surroundings in a process so energetic that it emits vast amounts of light.

So much so that quasars are some of the brightest objects in our sky, meaning even distant ones are visible from Earth.

As a general rule, the most luminous quasars indicate the fastest-growing supermassive black holes.

"We have discovered the fastest-growing black hole known to date. It has a mass of 17 billion Suns, and eats just over a Sun per day. This makes it the most luminous object in the known Universe," says Christian Wolf, an astronomer at the Australian National University (ANU) and lead author of the study published today in Nature Astronomy. The quasar, called J0529-4351, is so far away from Earth that its light took over 12 billion years to reach us.

The matter being pulled in toward this black hole, in the form of a disc, emits so much energy that J0529-4351 is over 500 trillion times more luminous than the Sun.

"All this light comes from a hot accretion disc that measures seven light-years in diameter -- this must be the largest accretion disc in the Universe," says ANU PhD student and co-author Samuel Lai.

Seven light-years is about 15,000 times the distance from the Sun to the orbit of Neptune.

And, remarkably, this record-breaking quasar was hiding in plain sight.

"It is a surprise that it has remained unknown until today, when we already know about a million less impressive quasars. It has literally been staring us in the face until now," says co-author Christopher Onken, an astronomer at ANU.

He added that this object showed up in images from the ESO Schmidt Southern Sky Survey dating back to 1980, but it was not recognised as a quasar until decades later.

Finding quasars requires precise observational data from large areas of the sky.

The resulting datasets are so large, researchers often use machine-learning models to analyse them and tell quasars apart from other celestial objects.

However, these models are trained on existing data, which limits the potential candidates to objects similar to those already known.

If a new quasar is more luminous than any other previously observed, the programme might reject it and classify it instead as a star not too distant from Earth.

An automated analysis of data from the European Space Agency's Gaia satellite passed over J0529-4351 for being too bright to be a quasar, suggesting it to be a star instead.

Source: ScienceDaily

Researchers pinpoint 5 subvariants of Alzheimer’s disease

 

• About 32 million people globally have Alzheimer’s disease.
• There is currently no cure for Alzheimer’s, however, some medications are available to treat symptoms and help slow disease progression.
• Researchers from Amsterdam University Medical Centers and Maastricht University have identified five biological variants directly related to Alzheimer’s disease.
• Scientists believe these findings may impact how future Alzheimer’s treatments are developed and prescribed.

Approximately 32 million peopleTrusted Source around the world have Alzheimer’s disease, a type of dementia causing memory loss and other types of cognitive issues.

There is currently no cure for Alzheimer’s disease, and researchers are still not completely sure what causesTrusted Source the condition. There are some medicationsTrusted Source available to help treat symptoms and potentially slow the progression of the disease.

Why look for Alzheimer’s biological variants? 

Although researchers do not know the exact cause behind Alzheimer’s disease, most agree the formation of beta-amyloid plaque build-upTrusted Source and tau tanglesTrusted Source characterize it.

Dr. Betty Tijms, associate professor of neurology, brain imaging, and neurodegeneration at Amsterdam University Medical Centers and lead author of this study, told Medical News Today that she and her team decided to look for biological processes other than beta-amyloid and tau that may affect Alzheimer’s disease.

They did that because genetic and tissue proteomic studies previously pointed out that other biological processes beyond amyloid and tau seem to be involved in Alzheimer’s disease.

“But this was difficult to study in patients because the brain is not easily accessible,” Dr. Tijms continued. “New techniques made it possible to measure many proteins in the cerebrospinal fluidTrusted Source, and the levels of those proteins provide a detailed picture of the processes that are ongoing in the brain.“

”So we made use of these innovations to study if certain subgroups of Alzheimer’s disease patients could be identified that share distinct underlying biological processes,” she added.

What are the 5 biological variants of Alzheimer’s disease?

For this study, Dr. Tijms and her team examined a little over 1,000 proteins in the cerebrospinal fluid of 419 people with Alzheimer’s disease. Through this examination, they discovered five biological variants within this group.

According to Dr. Tijms, the first subtype was characterized by abnormal outgrowth of nerve cells.

She explained:

“Outgrowth is a normal process in the brain when connections between nerve cells get damaged, for example, because of the clumping of amyloid-beta. But here we see that this process goes into overdrive, and does not seem to efficiently repair the connections. The immune system of this variant was not activated properly, which may [interfere] with the clearance of protein clumps.”

– Dr. Betty Tijms

“The second subtype had an overactive immune system, which aggravated the disease progression,” Dr. Tijms continued. “The third subtype had problems with the synthesis of proteins — RNA metabolism dysfunctionTrusted Source.”

”The fourth subtype had damage in the choroid plexusTrusted Source, which is the organ in the brain that produces cerebrospinal fluid,” she said. ”[And] the fifth subtype showed leakage of the blood-brain barrier.”

Now, researchers from Amsterdam University Medical Centers and Maastricht University in the Netherlands have identified five biological variants directly related to Alzheimer’s disease.

Scientists believe these findings — recently published in the journal Nature AgingTrusted Source — may impact how future Alzheimer’s treatments are developed and prescribed.

Surprising results may impact drug development

Both researchers found some of the discovered Alzheimer’s disease biological variants surprising.

“I was surprised by the subtype with dysregulated RNA metabolism because such processes have not been highlighted as a key factor in Alzheimer’s disease,” Dr. Pieter Jelle Visser, professor of molecular epidemiology of Alzheimer’s disease at Maastricht University in the Netherlands and senior author of this study, told MNT.

“It was surprising to see the new subtype with choroid plexus dysfunction,” Dr. Tijms also noted. “They had similar effects as [the] blood-brain barrier with low cerebrospinal fluid tau levels, for example, but no indication at all of leakage of blood proteins in the cerebrospinal fluid.“

“To me that indicates that these brain interfaces are really two different entities, with their own roles in Alzheimer’s disease,” she told us.

Both researchers believe these findings may change how Alzheimer’s medications are developed and prescribed in the future.

“The existence of these subtypes suggests that each subtype may need a different treatment,” Dr. Visser explained. “Future trials should take this into account and test their treatment in the subtypes that matched with the working mechanism of the drug.”

“Alternatively, each future Alzheimer’s disease trial should stratify on subtypes such that the subtypes that best respond to treatment can be identified,” he added. “Future trials may also take into account that side effects may differ between subtypes as well.”

Potential to accelerate intervention research

After reviewing this study, Dr. Karen D. Sullivan, a board-certified neuropsychologist, owner of I CARE FOR YOUR BRAIN, and Reid Healthcare Transformation Fellow at FirstHealth of the Carolinas in Pinehurst, NC, told MNT she found this research to be extremely hopeful, as it has been known for a long time that Alzheimer’s disease is an extremely heterogeneous subtype of neurodegenerative diseaseTrusted Source.

“Some patients have a slow and steady decline while others progress quickly,” she continued. “Some have predominantly memory symptoms while others experience primarily visual and spatial impairments. Identifying these five specific disease processes in Alzheimer’s disease is a necessary starting point [for] personalizing brain healthcare interventions.”

Dr. Jennifer Bramen, a senior research scientist at the Pacific Neuroscience Institute in Santa Monica, CA, also not involved in the current study agreed, saying: “There are many known risk factors for Alzheimer’s disease, and each patient has a unique risk profile. Patients exhibit diverse symptoms, progression timelines, and neurodegeneration patterns.”

“If the authors are correct in their hypothesis that different Alzheimer’s disease variants may respond differently to treatments, there’s an opportunity to reassess drugs that showed promise in earlier research but were not effective overall. If true, this has the potential to accelerate intervention research.”

– Dr. Jennifer Bramen

For the next steps in this research, Dr. Sullivan said she would like to see researchers find out if these five biological variants result in distinct clinical syndromes in people living with Alzheimer’s disease.

“What is the specific set of cognitive and behavior symptoms and the prognostic significance of these five variants — is there a cause-and-effect relationship?” she continued. “[And] the ultimate question — and here is where the hope lies — do these five variants respond preferentially to different experimental drugs or from different types of preventative or early interventions that keep the disease process from spreading throughout the brain?”

Source - Medical News Today

Alzheimer’s may be caused by a build-up of fat in brain cells

 

• Alzheimer’s disease is the most common form of dementia.
• The precise causes of the condition are still being fleshed out.
• For many years, scientists have concentrated on the role of proteins, but this focus is shifting.
• A new study concludes that lipid droplets in specific brain cells may be critical.

Characterized by neurodegeneration and a progressive loss of thinking skills, Alzheimer’s disease still holds many mysteries.

Globally, 55 million people are affected by dementia and by 2050 experts expect this figure to be 139 million.

Despite years of research, the precise mechanisms has been elusive.

A recent study, however, adds another piece to the puzzle.

For the past few decades, scientists have focused on protein build-up in neurons as the lynchpin of Alzheimer’s. So-called plaques and tangles coalesce in neurons and these hallmarks are linked to brain cell death.

Scientists recently designed drugs to clear these proteins, but they are not the silver bullet 
 that many people hoped for.

 Source

Trusted Source

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•  Highly respected journal
•  Expert written journal
•  Peer reviewed journal

Go to source

More recently, the focus has shifted toward the role of lipid droplets in brain cells.

Alzheimer’s disease and brain cells

A new studyTrusted Source published in the journal Nature examines links between Alzheimer’s risk genes and lipid droplets in microglia, which are immune cells in the brain.

The gene most strongly correlated with risk is the APOE gene. There are various forms of this gene and the one that carries the highest riskTrusted Source is APOE4.

APOE is involved in lipid processing and in people with Alzheimer’s, the gene’s activity is ramped upTrusted Source in microglia.

The increased activity by APOE causes lipid droplets to build up within the cells. However, to date, it has been unclear whether this buildup is protective, benign, or harmful.

Details from the study on brain cells and Alzheimer’s

To investigate, the researchers analyzed brain tissue from people who died with Alzheimer’s and a control group who did not have Alzheimer’s.

They measured gene expression within single cells to understand which genes are “turned on.”

Medical News Today spoke with one of the study’s authors, Michael Haney, PhD, an assistant professor in the department of pathology at Perelman School of Medicine at the University of Pennsylvania.

He was surprised that ACSL1, “a key regulator of lipid droplet formation,” was “one of the most upregulated genes in microglia.”

“This is interesting because Alois Alzheimer himself,” who first described the condition, “noted lipid bodies in glia in his patients’ brains over 100 years ago, but this has received little attention,“ Haney explained.

Next, the researchers used a staining technique to see where in the brain these lipid droplet-filled cells were situated.

They said they found that these lipid-containing cells were clustered around protein plaques. This could mean that plaques play a role in lipid accumulation.

To test this theory, the scientists treated microglia with amyloid fibrils, a major component of protein plaques associated with Alzheimer’s.

When they did this, there was a “strong increase” in lipid droplet accumulation, which was particularly pronounced in the presence of APOE4.

New Alzheimer’s research potential

Taken together, the authors believe their study “opens the possibility for a new hypothesis for [lipid droplet]-mediated pathogenesis” in Alzheimer’s.

Speaking with MNT, Haney summarized their results:

“We believe that when microglia encounter the protein buildup common in Alzheimer’s disease, a pro-inflammatory state is triggered in the microglia, which leads to the up-regulation of lipid synthesis enzymes and lipid accumulation in structures known as lipid droplets.”

While lipid accumulation in microglia is a novel finding, scientists have seen this response before. “It also occurs outside the brain when immune cells encounter bacteria,” explained Haney.

“We think a similar state is being triggered in these immune cells of the brain in response to plaques, leading to lipid accumulation and a pro-inflammatory, damaging state for these cells,” he added.

Not a new but an important theory

“This is an important study that highlights the importance of lipid metabolism in Alzheimer’s pathology,” saidAlfred Fonteh, PhD, an associate professor of neuroscience and head of the Biomarker and Neuro-disease Mechanism Lab in the Department of Neurosciences at the Huntington Research Institutes in California.

“​​With 50 percent of the brain composed of lipids and over 20 years of lipidomic analyses in my lab showing substantial changes in lipid pathways, I am not surprised by these results,” Fonteh, who wasn’t involved in the study, explained to Medical News Today.

Fon​teh added that the results of this study confirm what was already known with “the additional detail of a mechanism that can account for the role of lipids in Alzheimer’s.”

Does earlier work on Alzheimer’s support these findings?

Medical News Today also spoke with Hugo Bellen, PhD, and his colleagues from Baylor College of Medicine in Texas. They were not involved in this study, but Bellen’s lab has investigated the molecular basis of neurodegeneration for more than two decades.

They explained that studying postmortem tissue, while interesting and important, may not provide insights into how these conditions begin. The molecular changes that drive Alzheimer’s begin many years, if not decades, before obvious symptoms start.

By the time of death, many years later, unravelling what has happened in the brain is much more challenging.

Bellen’s researchTrusted Source concludes that damaging reactive oxygen species initially buildup because of mitochondrial issues in neurons. These trigger the production of lipids.

These toxic, peroxidated lipids are then transported via APOE to form lipid droplets in glial cells. These lipid droplets promote the breakdown of the peroxidated lipids, which protects the neurons from damage.

They have shown that the Alzheimer’s risk allele, APOE4, is a loss-of-function allele for this lipid transfer process. Loss of APOE — or any of the other proteins required for lipid transport in this pathway — leads to the demise of neurons as the toxic peroxidated lipids build up in the system.

An avenue to new Alzheimer’s treatments?

The authors of the new study hope that focusing on the role of lipid accumulation might help generate new ways to treat Alzheimer’s in the future.

However, there are challenges ahead.

“One of the main challenges in designing drugs to target these lipids or the Alzheimer’s risk genes that transport lipids is that these lipids and lipid-related proteins have important roles outside the brain in processes that you don’t want to disturb,” Haney said.

In other words, he said, we need to find a way to only target lipid accumulation in the right place, and not just lipids in general, because that would cause a range of other difficulties.

However, Haney is hopeful: “I think this might be possible with a better understanding of how this buildup occurs specifically in microglia and what damaging factors they might be secreting.”

Fonteh noted that “[l]ipid metabolism is extraordinarily complex and involves many other enzymes that may be altered in Alzheimer’s.”

“The important aspect of this study is that one size does not fit all,” he said. He expressed the hope that, eventually, we might open the door to more personalized treatment: “The challenge will be teasing out genetics, dietary, and other lifestyle factors when designing drugs.”

Haney also plans to continue this line of work.

“In my new lab, I plan on further characterizing the variety of diseases in which microglia accumulate lipid droplets, how they accumulate these lipids, and how they might damage nearby neurons,” he said.

Source - Medical News Today

How type 2 diabetes may be linked to Alzheimer's disease risk

 

• Researchers report that evidence suggests there is a relationship between type 2 diabetes and Alzheimer’s disease risk, something that some health professionals call type 3 diabetes.
• They said it’s possible that eating a high-fat diet might lead to higher levels of inflammation, which could increase dementia risk.
• They note that a healthy diet and participating in a healthy lifestyle might reverse the process and decrease the risk of developing Alzheimer’s disease.

There is growing evidence that type 2 diabetes and Alzheimer’s disease are linked, according to research completed at Texas A&M University and presented at the annual meeting of the American Society for Biochemistry and Molecular Biology.

In their findings, which haven’t been published yet in a peer-reviewed journal, researchers examined the relationship between the two diseases, using mice for their experiments.

The scientists said they traced a particular protein in the gut to find out how it influences brain processes. They reported that eating a high-fat diet suppresses a protein called jak3.

The mice without this protein experienced inflammation that began in the intestine and then moved to the liver and the brain. These mice developed Alzheimer’s-like symptoms, including cognitive impairment.

The potential link between Alzheimer’s and type 2 diabetes

The researchers suggest that it could be possible to reduce the risk of Alzheimer’s disease by controlling or avoiding type 2 diabetes.

The scientists note that previous research indicates that diet influences the development and severity of diabetes and, more recently, has been implicated in the risk of developing Alzheimer’s.

“Meta-analytic dataTrusted Source demonstrate a 56 percent increased risk for Alzheimer’s disease dementia among individuals with type 2 diabetes,” Narendra Kumar, PhD, the first author of the study and an associate professor of pharmaceutical sciences at Texas A&M, told Medical News Today. “Since there is a known link between diet and lifestyle with type 2 diabetes, we think, yes, diet and lifestyle can be considered as some of the major factors contributing to the progression toward Alzheimer’s disease.”

Although this study has not explored this connection and it is premature to draw any conclusions, Kumar does believe it is possible that this connection would be similar in other types of dementia.

How a leaky gut might be a factor

The researchers at Texas A&M say they have learned that the jak3 protein can lead to a leaky gut, resulting in low-grade chronic inflammation as well as type 2 diabetes, the decreased ability in the brain to clear toxic substances, and dementia-like symptoms.

A leaky gut is a condition in which gaps in the intestinal walls allow toxins and bacteria to leak out of the intestines and into the bloodstream. Not all health professionals recognize this as a distinct medical condition and further research is needed.

The researchers believe that stopping this process, including inflammation, is possible by eating a healthy diet and controlling blood sugar.

Ideally, they said, healthy eating and lifestyle habits can begin early enough to avoid high blood sugar or at least soon enough to reverse prediabetes.

The scientists suggest that these changes can reduce the risk of type 2 diabetes and Alzheimer’s disease.

Connecting type 2 diabetes and Alzheimer’s disease

Around 81% of people living with Alzheimer’s disease also have type 2 diabetes, according to a report by the Keck School of Medicine USC.

The risk of dementia corresponded with the diagnosis of diabetes – the younger the age of developing diabetes, the higher the risk of developing dementia.

Some scientists refer to the link between these two diseases as “type 3 diabetes.”

Because the liver metabolizes food, the researchers say it might be critical to the gut-brain connection.

It is not yet understood why this condition exists, but experts do know that high blood sugar or insulin can harm the brain and increase risk of Alzheimer’s, according to the Alzheimer’s Association.

The brain is the most energy-demanding organ — needing half of all the sugar energy in the body to function correctly. Both high and low blood sugar can damage blood vessels in the brain, according to the Centers for Disease Control and PreventionTrusted Source.

When blood sugar levels are outside of normal range, it can damage nerve and blood vessels in the brain, causing problems with memory, learning, mood, weight gain, and hormonal changes. Over time it can lead to Alzheimer’s disease.

Treating type 2 diabetes

The goal of treatment for type 2 diabetes is to prevent it from causing other health problems, according to the National Institutes of HealthTrusted Source.

“Severe obesity is deadly. People’s bodies are 10 to 20 years older than their chronological age. Heart disease is the biggest killer,” said Dr. Mitchell Roslin, the chief of bariatric surgery at Northwell Lenox Hill Hospital in New York who was not involved in the study.

There are several effective treatments, according to Roslin.

“Bariatric surgery is a tool that makes eating less, eating healthier foods, and activity more feasible,” Roslin told Medical News Today. “It is still going to be subject to socioeconomic factors and the environment and stresses people face.”

He added that in the past few years, federal regulators have approved several weight loss medications that can help reduce the risk of diabetes. Tirzepatide (Mounjaro, Zepbound) and semaglutide (Ozempic, Wegovy) work to reduce feelings of hunger and help a person lose weight, which can help control type 2 diabetes.

Diet, exercise, and other lifestyle factors are also important, according to experts.

“Diet and lifestyle changes to address weight is highly effective in reducing your risk for diabetes as well as controlling it,” said Lauren Sepe, a clinical nutritionist at the Kellman Wellness Center in New York who was not involved in the study. “Although the advent of these new and highly effective medications are very helpful to many people, there is a lot of people can do on their own to address their condition.”

“I recommend not only a diet low in carbohydrates and added sugars, but also a diet that addresses inflammation,” Sepe told Medical News Today.

Sepe offered these tips:

• Focus on lean protein, free range protein, wild caught fish, and seafood
• Grass-fed meat in moderation. Grass-fed meat has been shown to contain a higher amount of naturally anti-inflammatory Omega-3 fatty acids, as compared to the conventional meats which are in higher in pro-inflammatory Omega-6 fatty acids
• Healthy fats, such as those found in olive oil, coconut oil, and avocados
• Plenty of non-starchy vegetables as these vegetables tend to be higher in carbohydrate content
• Eggs
• Nuts and seeds, in moderation. They are nutrient dense and contain healthy fats but tend to be higher in calories
• Low sugar fruits in moderation, including apples, citrus fruits, berries, and melons
• Dairy in moderation, preferably good quality, organic versions.

Source - Medical News Today