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A brief illustration of the main cellular processes and biological pathways that contribute to the development of Pancreatic cancer, with emphasis on the genetic mutations and cellular alterations. Credit: Current Oncology (2022). Doi: https://doi.org/10

A brief illustration of how each diagnostic test contributes to cancer detection, progression assessment, as well as treatment decision-making, and how they complement each other in clinical settings to provide a thorough evaluation of pancreatic cancer.

AI models have the potential not only to spot pancreatic cancer at an early stage, but also to predict the deadly disease’s prognosis, say scientists

SHARJAH, EMIRATE OF SHARJAH, UNITED ARAB EMIRATES, June 30, 2025 /EINPresswire.com/ — Oncologists utilizing Artificial Intelligence (AI) in their tests to spot pancreatic cancer at an early stage can also gain an overall picture of how the deadly disease is bound to develop, scientists from the University of Sharjah have revealed in a new study.

Although still at its initial stage, the AI-enabled prognosis, the scientists say, has the potential to pave the way for the provision of individualized healthcare and treatment of pancreatic cancer patients.

The scientists, who describe their findings in Beni-Suef University Journal of Basic and Applied Sciences, arrived at the groundbreaking conclusion following a comprehensive review of pancreatic cancer-related scientific literature. https://doi.org/10.1186/s43088-025-00610-4

Due to its high mortality rate, pancreatic cancer poses a serious health concern, with 467,409 deaths reported worldwide in 2022 and 510,992 new cases. Researchers often refer to pancreatic cancer as the ‘king’ of all cancers due to the exceptional ability of its cancerous cells to quickly spread to other parts of the body if not detected at an early stage.

“Nevertheless, due to several factors, including the lack of distinct molecular markers and clinical symptoms, the disease tends to be detected at an advanced stage, rendering surgical interventions futile,” the authors warn. ”For this reason, early detection and precise stratification of pancreatic cancer stages are crucial for enhancing therapeutic outcomes.”

In their study, the scientists provide what they claim to be “a concise overview” of how AI is used in the diagnosis, prognosis, and treatment of pancreatic cancer.

“Utilizing AI for preliminary testing can significantly enhance the prognosis of those who have been diagnosed with pancreatic cancer,” they write. “Advances in AI-driven image analysis have the potential to transform computer-aided diagnostic systems, aiding doctors in establishing precise and reliable assessments.”

The researchers’ extensive review of the literature dwells on numerous aspects of AI and its multiple uses in handling cases of pancreatic cancer.

One important aspect for the scientists is multicomics, which requires the combination and analysis of different data types, along with professionals and scientists, to acquire a thorough and deep understanding of a complex and deadly disease like pancreatic cancer.

They note that “it is crucial to recognize the significance of AI in multiomics domains. The healthcare industry is at the forefront of a new era, driven by technological and scientific improvements, facilitated by the integration of AI in healthcare.

“This progress can only be made through the efforts of clinicians, scientists, data analysts, and technicians. Although computer systems have several limits, they are anticipated to contribute to substantial breakthroughs soon, owing to their amazing processing powers.”

The authors endow AI models with a high ability to spot pancreatic tumors at their earliest stages, helping doctors to correctly assess the risks for patients, and then provide the associated healthcare and draw plans for long-term treatment.

They call for a better grasp and control of these models, as they are not easy to operate and understand. They show that the plethora of AI-based solutions about pancreatic cancer detection, prognosis, and treatment have “made clinical use a bit sophisticated, whereby without understanding and clear interpretation, doctors cannot critically evaluate the output of these algorithms in terms of their applicability and reliability.”

Despite the sophistication associated with AI applications, the authors report that researchers have been exerting considerable efforts to develop a variety of approaches to make them accessible to healthcare professionals and at the same time gain the confidence of patients about their effectiveness.

They predict a promising future for upcoming AI tools, which they believe can be employed with much less sophistication due to the emergence of a new frontier in artificial intelligence called explainable AI that will make the tools easily accessible for clinical adoption.

They reveal that cancer researchers are “creating and applying explainable AI methods, including feature relevance ratings, infographics, and natural language explanations to interpret AI predictions.”

They highly commend the new Machine Learning models to identify pancreatic cancer at an early stage, with implications for a significant reduction in the morbidity and mortality rates.

The application of methods employing the Internet of Things have recently caught the attention of oncological researchers who, according to the authors, are expected to revolutionize pancreatic cancer detection, prognosis, and treatment.

“AI ought to help oncologists create personalized treatment regimens by combining patient-specific data. It is being utilized to predict how patients react to therapies like immunotherapy, chemotherapy, radiation therapy, and surgery,” they write.

In their recommendations, the authors call for more AI-based pancreatic cancer research to eventually build “semi-autonomous models that reduce clinician stress, boost productivity, or be fully autonomous.”

LEON BARKHO
University Of Sharjah
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The pursuit of a cure for Alzheimer’s disease is becoming an increasingly competitive and contentious quest with recent years witnessing several important controversies.

In July 2022, Science magazine reported that a key 2006 research paper, published in the prestigious journal Nature, which identified a subtype of brain protein called beta-amyloid as the cause of Alzheimer’s, may have been based on fabricated data.

One year earlier, in June 2021, the US Food and Drug Administration had approved aducanumab, an antibody-targeting beta-amyloid, as a treatment for Alzheimer’s, even though the data supporting its use were incomplete and contradictory.

Some physicians believe aducanumab never should have been approved, while others maintain it should be given a chance.

Related: New Link Connects Herpes to Alzheimer’s. Here’s What We Know.

With millions of people needing an effective treatment, why are researchers still fumbling in this quest for a cure for what is arguably one of the most important diseases confronting humankind?

Escaping the beta-amyloid rut

For years, scientists have been focused on trying to come up with new treatments for Alzheimer’s by preventing the formation of brain-damaging clumps of this mysterious protein called beta-amyloid.

In fact, we scientists have arguably got ourselves into a bit of an intellectual rut concentrating almost exclusively on this approach, often neglecting or even ignoring other possible explanations.

Regrettably, this dedication to studying the abnormal protein clumps has not translated into a useful drug or therapy. The need for a new “out-of-the-clump” way of thinking about Alzheimer’s is emerging as a top priority in brain science.

My laboratory at the Krembil Brain Institute, part of the University Health Network in Toronto, is devising a new theory of Alzheimer’s disease.

Based on our past 30 years of research, we no longer think of Alzheimer’s as primarily a disease of the brain. Rather, we believe that Alzheimer’s is principally a disorder of the immune system within the brain.

The immune system, found in every organ in the body, is a collection of cells and molecules that work in harmony to help repair injuries and protect from foreign invaders.

When a person trips and falls, the immune system helps to mend the damaged tissues. When someone experiences a viral or bacterial infection, the immune system helps in the fight against these microbial invaders.

The exact same processes are present in the brain. When there is head trauma, the brain’s immune system kicks into gear to help repair. When bacteria are present in the brain, the immune system is there to fight back.

Alzheimer’s as autoimmune disease

We believe that beta-amyloid is not an abnormally produced protein, but rather is a normally occurring molecule that is part of the brain’s immune system. It is supposed to be there.

When brain trauma occurs or when bacteria are present in the brain, beta-amyloid is a key contributor to the brain’s comprehensive immune response. And this is where the problem begins.

Because of striking similarities between the fat molecules that make up both the membranes of bacteria and the membranes of brain cells, beta-amyloid cannot tell the difference between invading bacteria and host brain cells, and mistakenly attacks the very brain cells it is supposed to be protecting.

This leads to a chronic, progressive loss of brain cell function, which ultimately culminates in dementia – all because our body’s immune system cannot differentiate between bacteria and brain cells.

When regarded as a misdirected attack by the brain’s immune system on the very organ it is supposed to be defending, Alzheimer’s disease emerges as an autoimmune disease.

There are many types of autoimmune diseases, such as rheumatoid arthritis, in which autoantibodies play a crucial role in the development of the disease, and for which steroid-based therapies can be effective. But these therapies will not work against Alzheimer’s disease.

The brain is a very special and distinctive organ, recognized as the most complex structure in the Universe.

In our model of Alzheimer’s, beta-amyloid helps to protect and bolster our immune system, but unfortunately, it also plays a central role in the autoimmune process that, we believe, may lead to the development of Alzheimer’s.

Though drugs conventionally used in the treatment of autoimmune diseases may not work against Alzheimer’s, we strongly believe that targeting other immune-regulating pathways in the brain will lead us to new and effective treatment approaches for the disease.

Other theories of the disease

In addition to this autoimmune theory of Alzheimer’s, many other new and varied theories are beginning to appear. For example, some scientists believe that Alzheimer’s is a disease of tiny cellular structures called mitochondria – the energy factories in every brain cell.

Mitochondria convert oxygen from the air we breathe and glucose from the food we eat into the energy required for remembering and thinking.

Some maintain that it is the end-result of a particular brain infection, with bacteria from the mouth often being suggested as the culprit. Still others suggest that the disease may arise from an abnormal handling of metals within the brain, possibly zinc, copper, or iron.

It is gratifying to see new thinking about this age-old disease. Dementia currently affects more than 50 million people worldwide, with a new diagnosis being made every three seconds.

Often, people living with Alzheimer’s disease are unable to recognize their own children or even their spouse of more than 50 years.

Alzheimer’s is a public health crisis in need of innovative ideas and fresh directions.

For the well-being of the people and families living with dementia, and for the socioeconomic impact on our already stressed health-care system coping with the ever-escalating costs and demands of dementia, we need a better understanding of Alzheimer’s, its causes, and what we can do to treat it and to help the people and families who are living with it.

Donald Weaver, Professor of Chemistry and Director of Krembil Research Institute, University Health Network, University of Toronto

This article is republished from The Conversation under a Creative Commons license. Read the original article.

An earlier version of this article was published in September 2022.

Brain health has become a popular topic as scientists continue to study the brain in more depth. And while there is still much to learn about the brain, one thing we do know is that dementia is on the rise. We recently reported on a study that suggests that new dementia cases may double from half a million to a million per year by the year 2060. Since we know more about the brain and how to take care of it than we did just a few years ago, this estimation is pretty astonishing.

Dementia is a general term for a loss of memory, language, problem-solving skills and other abilities that are severe enough to interfere with everyday life. Alzheimer’s disease is the most common type of dementia. 

We know that nutrition plays a large role in brain health. There’s even a diet designed specifically to provide brain-healthy nutrients, called the MIND diet. Scientists also consider specific foods to see if there is any correlation between them and decreased disease risk. This is what researchers from Japan did regarding green tea and dementia risk. They recently published their findings in The Journal of Nutrition, Health and Aging. Let’s break down what they found.

How Was This Study Conducted?

Researchers drew data from a long-running Japanese study called the Murakami study. This study included 13,660 people, about 52% women with an average age of 59. 

Some of the demographics adjusted for during statistical analysis included sex, age, BMI, physical activity, smoking status, alcohol consumption, education level, marital status and medical history. Participants also filled out food frequency questionnaires asking how much and how often certain foods and beverages were consumed, including tea and coffee.  Baseline data was collected between 2011 and 2013, and the average follow-up time for each participant was 11.5 years. 

For tea and coffee, participants were given the following options for their intake: <1 cup per week, 1-2 cups per week, 3-4 cups per week, 5-6 cups per week, 1 cup per day, 2-3 cups per day, 4-6 cups per day, 7-9 cups per day, and 10 cups per day. Options were also given for canned and bottled tea and coffee, and amounts were calculated into the total intake. 

It’s important to note that “a cup” can be interpreted as different amounts in studies and, in this case, is not equal to our American-sized measuring cup. For this reason, researchers calculated consumption into milliliters per day and then placed participants into one of four quartiles (categories). Q1 drank <94 mL of green tea per day, Q2 drank 94-299 mL/day, Q3 drank 300-599 mL/day and Q4 drank ≥ 600 mL/day. 

Because they were looking specifically for associations between tea and dementia risk, researchers also gathered data regarding dementia from Japan’s long-term care insurance (LTCI) database. In the LTCI, physicians assess the degree of dementia and classify patients into six ranks ranging from no dementia (0) to severe dementia-related behavioral impairment and cognitive impairment requiring treatment (V)—basically using Roman numerals, plus the number 0. Those with rank II (moderate dementia-related behavioral disturbances and cognitive dysfunction with mild dependence) or higher are considered to have dementia.

What Did This Study Show?

After running statistical analyses, researchers found that those in the higher quartiles for green tea intake had a lower risk of dementia. Specifically, those in the highest quartile, who drank at least 600 mL (or 20 fluid ounces) per day, had a 25% lower risk of dementia compared to those in the first quartile. 

They also broke it down by cups of green tea consumed. Participants saw about a 5% reduction in dementia risk for each cup increase in green tea. For example, if someone averaged a cup of green tea a day, they may decrease their risk of dementia by 5%. For someone who drinks 2 cups a day, the reduction in risk goes to 10%. Keep in mind, though, that these cups are not what we consider a measuring cup amount—they’re actually closer to about ½ cup. As an example, Q4 drank at least 600 mL of green tea a day, which is equal to about 2.5 American measuring cups, and reduced their risk of dementia by 25% compared to those in Q1.

Because there is some evidence that coffee may decrease dementia risk, researchers were curious to know if those who drank both coffee and green tea might lower their risk even more. Turns out, unlike those who drank a lot of green tea, adding high levels of coffee in addition to green tea did not have the same effects as green tea alone, and showed no reduction in dementia risk. 

Researchers propose a couple of possible reasons for this. First, drinking both green tea and coffee in high doses might have a sort of overdose effect, especially regarding caffeine. As an example, green tea contains 20 mg of caffeine per 100 mL dose, and coffee contains 60 mg of caffeine for the same amount. During the combined portion of this trial, participants in Q4 consumed at least 600 mL/day of green tea and 300 mL/day of coffee, which averages out to 300 mg of caffeine per day. And some were drinking well beyond these amounts. The current recommendation for caffeine is no more than 400 mg/day, so those in Q4 were definitely near or beyond that amount.

Researchers also note that coffee and tea contain different plant compounds and that they may counteract each other. But they seemed to lean more into the caffeine theory.

There are a few limitations to this study. One is that participants’ cognitive status was not assessed at baseline. So there’s a chance that those who had lower cognitive function at the start of the study drank less green tea. If this is true, then the association between green tea and reduced risk of dementia would be weaker. Also, because green tea consumption was estimated based on self-reports, it leaves room for bias and inaccuracies. Lastly, the type of dementia wasn’t investigated, so they can’t say which types of dementia green tea may reduce. Researchers do note, however, that because it’s estimated that Alzheimer’s disease makes up about two-thirds of dementia cases, green tea may help reduce the risk of Alzheimer’s. 

How Does This Apply to Real Life?

All types of true teas—green, black, white and oolong—are loaded with antioxidants. They are, after all, plants, and all plants contain antioxidants. But compared to the others, green tea has been shown to have the highest levels of catechins, a specific type of flavonoid antioxidant, providing about four times more catechins than black tea. One of these catechins is epigallocatechin3-gallate (EGCG), which researchers note in previous studies has been linked to reduced Alzheimer’s risk. Reasons for this may be due to EGCG’s ability to reduce inflammation, including in the brain, plus reduce amyloid-beta and tau-tangle accumulation, both of which are implicated in Alzheimer’s disease. 

That’s not to say that other teas don’t have their own benefits. For example, black tea may help you live longer, and ginger tea can help ease an upset stomach and reduce arthritis pain. Mint tea has been shown to have digestive, respiratory and mental health benefits, as well as antimicrobial and antiviral properties.

Besides brain health, green tea has also been associated with lower inflammation, better digestion, less bloating, improved blood sugar and cholesterol levels, and reduced risk of cancer. 

It’s easy to add green tea to your life. Simply brew up a cup. Ideally, we recommend using loose-leaf tea and steeping it in a tea strainer. The reason for this is that some tea bags have been shown to contain microplastics. These tiny particles may end up steeping from the bag into your cup of tea and ultimately into your body, including your brain. If you’re looking to limit your microplastic exposure, a tea strainer may be the best steeping option. 

Plain green tea is best, but adding a small amount of honey or sugar or a touch of milk is fine if that’s how you prefer it. Just be mindful of how much you add, since too much added sugar has been associated with worse brain health, including dementia. If you want to get to zero additions in your tea, take your usual amount of sweetener and/or cream and begin reducing that amount each week until you’re at nothing but the tea. Doing this gradually will help your taste buds adjust. It’s also important to point out that the longer you steep your tea, the more bitter it’s likely to become. If you don’t care for the bitterness, go with shorter steeping times.

If you’re not a tea drinker (and even if you are) and want the benefits of catechins, there are a few options for you. Dark chocolate, cherries and berries, including blackberries, raspberries and strawberries, are rich in these powerful plant compounds. Dark chocolate and walnuts make a great brain-healthy snack. And cherries and berries are amazing in smoothies, including our Cherry-Mocha Smoothie,  Raspberry-Kefir Power Smoothie and our Berry-Green Tea Smoothie, which provides catechins from both berries and green tea. 

If you’re ready to really dive into eating for brain health, then you’ll want to try our 30-Day MIND Diet Meal Plan for Cognitive Health or our Simple 7-Day Cognitive Health Meal Plan. 

Our Expert Take

This study suggests that higher consumption of green tea is associated with reduced risk of dementia, compared to those with little to no green tea intake. Other lifestyle habits also contribute to brain health, including overall diet, physical activity, managing stressors and getting plenty of quality sleep. If this feels overwhelming and you’re not sure where to start, choose an area you’re likely to have success in. Adding a couple of cups of green tea each day could be an easy addition and starting point.

Inflammation, long considered a hallmark of aging, may not be a universal human experience, according to a new study from Columbia University Mailman School of Public Health. The research suggests that “inflammaging”-chronic, low-grade inflammation associated with aging-appears to be a byproduct of industrialized lifestyles and varies significantly across global populations. The findings are published in Nature Aging.

Researchers analyzed data from four populations: two industrialized groups-the Italian InCHIANTI study and the Singapore Longitudinal Aging Study (SLAS)-and two Indigenous, non-industrialized populations-the Tsimane of the Bolivian Amazon and the Orang Asli of Peninsular Malaysia. While the inflammaging signature was similar between the two industrialized populations, it did not hold in the Indigenous groups, where inflammation levels were largely driven by infection rather than age.

“In industrialized settings, we see clear links between inflammaging and diseases like chronic kidney disease,” said lead author Alan Cohen, PhD, associate professor of Environmental Health Sciences at Columbia Mailman School and faculty member of the Butler Columbia Aging Center. “But in populations with high infection rates, inflammation appears more reflective of infectious disease burden than of aging itself.”

Interestingly, while the indigenous populations, particularly the Tsimane, had high constitutive levels of inflammation, these did not increase with age and, crucially, did not lead to the chronic diseases that plague industrialized societies. In fact, most chronic diseases- diabetes, heart disease, Alzheimer’s, etc.-are rare or largely absent in the Indigenous populations, meaning that even when young Indigenous people have profiles that look similar on the surface to those of older industrialized adults, these profiles do not lead to pathological consequences.

“These findings really call into question the idea that inflammation is bad per se,” said Cohen. “Rather, it appears that inflammation-and perhaps other aging mechanisms too-may be highly context dependent. On the one hand, that’s challenging, because there won’t be universal answers to scientific questions. On the other, it’s promising, because it means we can intervene and change things.”

The study used a panel of 19 cytokines-small immune-signaling proteins-to assess inflammation patterns. While these markers aligned with aging in the Italian and Singaporean datasets, they did not replicate among the Tsimane and Orang Asli, whose immune systems were shaped by persistent infections and distinct environmental exposures.

Key findings include:

• Approximately 66 percent of Tsimane had at least one intestinal parasitic infection; over 70 percent of Orang Asli had a prevalent infection.
• Inflammaging markers were strongly linked to chronic disease in industrialized populations, but not in Indigenous groups.
• The study challenges the assumption of universal aging biomarkers, suggesting instead that immune-aging processes are population-specific and heavily influenced by the exposome-the totality of environmental, lifestyle, and infectious exposures.

“These results point to an evolutionary mismatch between our immune systems and the environments we now live in,” Cohen explained. “Inflammaging may not be a direct product of aging, but rather a response to industrialized conditions.”

The authors call for a reevaluation of how aging and inflammation are measured across populations and emphasize the need for standardized, context-aware tools. “Factors like environment, lifestyle-such as high physical activity or a very low-fat diet-and infection may all influence how the immune system ages,” said Cohen. “Understanding how these elements interact could help develop more effective global health strategies.”

Co-authors are listed in the manuscript.

The study was supported by the Impetus program, the French National Research Agency (ANR) under the Investments for the Future (Investissements d’Avenir) program, grant ANR-17-EURE-0010; the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under project ID 499552394 (SFB 1597/1) and grant HE9198/1-1, and the Intramural Research Program of the NIH, National Institute on Aging.