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New insights into role of high blood pressure in development of dementia

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For the first time, researchers have identified specific regions of the brain that are damaged by high blood pressure and may contribute to a decline in mental processes and the development of dementia.

High blood pressure is known to be involved in causing dementia and damage to brain function. The study, which is published in the European Heart Journal shows how this happens. 

It gathered information from a combination of magnetic resonance imaging (MRI) of brains, genetic analyses and observational data from thousands of patients to look at the effect of high blood pressure on cognitive function. The researchers then checked their findings in a separate, large group of patients in Italy.

Tomasz Guzik, Professor of Cardiovascular Medicine, at the University of Edinburgh (UK) and Jagiellonian University Medical College, Krakow (Poland), who led the research, said: “By using this combination of imaging, genetic and observational approaches, we have identified specific parts of the brain that are affected by increases in blood pressure, including areas called the putamen and specific white matter regions. We thought these areas might be where high blood pressure affects cognitive function, such as memory loss, thinking skills and dementia. When we checked our findings by studying a group of patients in Italy who had high blood pressure, we found that the parts of the brain we had identified were indeed affected.

“We hope that our findings may help us to develop new ways to treat cognitive impairment in people with high blood pressure. Studying the genes and proteins in these brain structures could help us understand how high blood pressure affects the brain and causes cognitive problems. Moreover, by looking at these specific regions of the brain, we may be able to predict who will develop memory loss and dementia faster in the context of high blood pressure. This could help with precision medicine, so that we can target more intensive therapies to prevent the development of cognitive impairment in patients most at risk.”

High blood pressure is common and occurs in 30. per cent of people worldwide, with an additional 30 per cent showing the initial stages of the disease. Studies have shown that it affects how well the brain works and that it can cause long-term changes. However, until now it was not known exactly how high blood pressure damages the brain and which specific regions are affected.

In research co-funded by the European Research Council, the British Heart Foundation and the Italian Ministry of Health, Prof. Guzik and an international team of researchers used brain MRI imaging data from over 30,000 participants in the UK Biobank study, genetic information from genome-wide association studies (GWAS) from UK Biobank and two other international groups (COGENT and the International Consortium for Blood Pressure). They used a technique called Mendelian randomisation, to see if high blood pressure was actually the cause of changes to specific parts of the brain rather than just being associated with these changes.

“Mendelian randomisation is a way of using genetic information to understand how one thing affects another,” said Professor Guzik. 

“In particular, it tests if something is potentially causing a certain effect, or if the effect is just a coincidence. It works by using a person’s genetic information to see if there is a relationship between genes predisposing to higher blood pressure and outcomes. If there is a relationship, then it is more likely that the high blood pressure is causing the outcome. This is because genes are randomly passed down from parents, so they are not influenced by other factors that could confuse the results.

“In our study, if a gene that causes high blood pressure is also linked to certain brain structures and their function, then it suggests that high blood pressure might really be causing brain dysfunction at that location, leading to problems with memory, thinking and dementia.”

 The researchers found changes to nine parts of the brain were related to higher blood pressure and worse cognitive function. These included the putamen, which is a round structure in the base of the front of the brain, responsible for regulating movement and influencing various types of learning. 

Other areas affected were the anterior thalamic radiation, anterior corona radiata and anterior limb of the internal capsule, which are regions of white matter that connect and enable signalling between different parts of the brain. The anterior thalamic radiation is involved in executive functions, such as the planning of simple and complex daily tasks, while the other two regions are involved in decision-making and the management of emotions.

The changes to these areas included decreases in brain volume and the amount of surface area on the brain cortex, changes to connections between different parts of the brain, and changes in measures of brain activity.

First author of the study, Associate Professor Mateusz Siedlinski, also a researcher at the Jagiellonian University Medical College, said: “Our study has, for the first time, identified specific places in the brain that are potentially causally associated with high blood pressure and cognitive impairment. This was uniquely possible thanks to the availability of data from UK Biobank, including MRI brain images, and thanks to previous research identifying genetic variants that affect the structure and function of over 3000 areas of the brain.”

 Co-author of the study, Professor Joanna Wardlaw, Head of Neuroimaging Sciences at the University of Edinburgh, added: “It has been known for a long time that high blood pressure is a risk factor for cognitive decline, but how high blood pressure damages the brain was not clear. This study shows that specific brain regions are at particularly high risk of blood pressure damage, which may help to identify people at risk of cognitive decline in the earliest stages, and potentially to target therapies more effectively in future.”

Limitations of the study include that participants in the UK Biobank study are mainly white and middle-aged, so it might not be possible to extrapolate the findings to older people.

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Quit Googling to stave off dementia onset, expert urges

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Resisting the temptation to search the web for information that could otherwise be recalled be exercising your brain could help to reduce the risk of dementia.

That is according to Canadian academic Professor Mohamed I. Elmasry who believes simple daily habits such as afternoon naps, memory ‘workouts’ and not reaching for a smartphone can increase the odds of healthy aging.

His new book, iMind: Artificial and Real Intelligence, says the focus has shifted too far away from RI (natural, or real) intelligence in favour of AI (machine, or artificial) intelligence. Elmasry instead calls us to nurture our human mind which, like smartphones, has ‘hardware’, ‘software’ and ‘apps’ but is many times more powerful – and will last much longer with the right care.

Professor Elmasry, an internationally recognised expert in microchip design and AI, was inspired to write the book after the death of his brother-in-law from Alzheimer’s and others very close to him, including his mother, from other forms of dementia.

Although he says that smart devices are ‘getting smarter all the time’, he argues in iMind that none comes close to ‘duplicating the capacity, storage, longevity, energy efficiency, or self-healing capabilities of the original human brain-mind’.

He writes that: “The useful life expectancy for current smartphones is around 10 years, while a healthy brain-mind inside a healthy human body can live for 100 years or longer.

“Your brain-mind is the highest-value asset you have, or will ever have. Increase its potential and longevity by caring for it early in life, keeping it and your body healthy so it can continue to develop.

“Humans can intentionally develop and test their memories by playing ‘brain games,’ or performing daily brain exercises. You can’t exercise your smartphone’s memory to make it last longer or encourage it to perform at a higher level.”

In iMind: Artificial and Real Intelligence Professor Elmasry shares an anecdote about his grandchildren having to use the search engine on their smartphones to name Cuba’s capital—they had just spent a week in the country with their parents.

The story illustrates how young people have come to rely on AI smartphone apps instead of using their real intelligence (RI), he says, adding: “A healthy memory goes hand-in-hand with real intelligence. Our memory simply can’t reach its full potential without RI.”

Published by Routledge, iMind: Artificial and Real Intelligence includes extensive background on the history of microchip design, machine learning and AI and their role in smartphones and other technology.

The book also explains how both AI and human intelligence really work, and how brain function links the mind and memory. It compares the human mind and brain function with that of smartphones, ChatGPT and other AI-based systems.

Drawing on comprehensive existing research, iMind aims to narrow the knowledge gap between real and artificial intelligence, to address the current controversy around AI, and to inspire researchers to find new treatments for Alzheimer’s, other neurodegenerative conditions and cancer.

It argues that current or even planned AI cannot match the capabilities of the human brain-mind for speed, accuracy, storage capacity and other functions. Healthy aging, Professor Elmasry notes, is as important as climate change but doesn’t attract a fraction of the publicity.

He calls for policymakers to adopt a series of key reforms to promote healthy aging. Among such changes, he suggests that bingo halls could transition from their sedentary entertainment function to become active and stimulating learning centers.

As well as napping to refresh our memories and other brain and body functions, he also outlines a series of practical tips to boost brain power and enhance our RI (Real Intelligence).

These include building up ‘associative’ memory – the brain’s ‘dictionary of meaning’ where it attaches new information to what it already knows. Try reading a book aloud, using all of your senses instead of going on autopilot and turning daily encounters into fully-lived experiences.

Other techniques include integrating a day for true rest into the week, reviewing your lifestyle as early as your 20s or 30s, adopting a healthy diet, and eliminating or radically moderating alcohol consumption to reduce the risk of dementia.

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Study reveals strong links between the quality of diet and cognitive ability

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Eating a high-quality diet in youth and middle age could help keep your brain functioning well in your senior years, according to new preliminary findings from a study that used data collected from over 3,000 people followed for nearly seven decades.

The research adds to a growing body of evidence that a healthy diet could help ward off Alzheimer’s disease and age-related cognitive decline. Whereas most previous research on the topic has focused on eating habits of people in their 60s and 70s, the new study is the first to track diet and cognitive ability throughout the lifespan — from age 4 to 70 — and suggests the links may start much earlier than previously recognized.

“These initial findings generally support current public health guidance that it is important to establish healthy dietary patterns early in life in order to support and maintain health throughout life,” said Kelly Cara, PhD, a recent graduate of the Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy at Tufts University.

“Our findings also provide new evidence suggesting that improvements to dietary patterns up to midlife may influence cognitive performance and help mitigate, or lessen, cognitive decline in later years.”

Cognitive performance, or thinking ability, can keep improving well into middle age, but typically begins to decline after age 65. More severe conditions such as dementia can also develop alongside aging-related declines. Researchers say that eating a healthy diet — in particular, a diet rich in plant-based foods that contain high levels of antioxidants and mono- and polyunsaturated fats — can support brain health by reducing oxidative stress and improving blood flow to the brain.

For the new research, scientists used data from 3,059 U.K. adults who were enrolled as children in a study called National Survey of Health and Development. Members of the cohort, called the 1946 British Birth Cohort, have provided data on dietary intakes, cognitive outcomes and other factors via questionnaires and tests over the course of more than 75 years.

Analysing participants’ dietary intakes at five timepoints in relation to their cognitive ability at seven timepoints, researchers found that dietary quality was closely linked with trends in general, or “global,” cognitive ability. For example, only about 8% of people with low-quality diets sustained high cognitive ability and only about 7% of people with high-quality diets sustained low cognitive ability over time compared with their peers.

Cognitive ability can have important impacts on quality of life and independence as we age. For example, at age 68-70, participants in the highest cognitive group showed a much higher retention of working memory, processing speed and general cognitive performance compared to those in the lowest cognitive group. In addition, nearly one-quarter of participants in the lowest cognitive group showed signs of dementia at this timepoint while none of those in the highest cognitive group showed signs of dementia.

While most people saw steady improvements in their dietary quality throughout adulthood, the researchers noted that slight differences in diet quality in childhood seemed to set the tone for later life dietary patterns, for better or worse. “This suggests that early life dietary intakes may influence our dietary decisions later in life, and the cumulative effects of diet over time are linked with the progression of our global cognitive abilities,” said Cara.

To assess diet quality, the researchers used the 2020 Healthy Eating Index, which measures how closely one’s diet aligns with the 2020-2025 Dietary Guidelines for Americans. Study participants who sustained the highest cognitive abilities over time relative to their peers tended to eat more recommended foods such as vegetables, fruits, legumes and whole grains and less sodium, added sugars and refined grains.

“Dietary patterns that are high in whole or less processed plant-food groups including leafy green vegetables, beans, whole fruits and whole grains may be most protective,” said Cara. “Adjusting one’s dietary intake at any age to incorporate more of these foods and to align more closely with current dietary recommendations is likely to improve our health in many ways, including our cognitive health.”

Since the study participants were predominantly Caucasian individuals from across the U.K., the researchers said that further research would be needed to determine whether the results would apply to populations with greater racial, ethnic and dietary diversity. They also noted that changes in study focus and protocols over the course of the long-running study created some gaps and inconsistencies in data collection. Despite these limitations, however, the researchers were able to create global cognitive ability percentile rank scores using data from multiple cognitive domains to evaluate how participants compared to their peers at each age and over time.

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Research unveils new insights into osteoporosis development

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Researchers from Osaka University have identified a gene underlying the development of osteoporosis, and have developed a new mouse model, pointing the way for future treatments and a greater understanding of this disease.

Osteoporosis — weakening of the bones with age — affects millions worldwide, and this figure is increasing annually as the global population ages.

It is associated with the ageing, or ‘senescence’, of bone cells, but the underlying cell types and mechanisms were unclear. Now, however, a research team from Osaka University has identified a key osteoporosis-related gene, Men1, and developed a new animal model of this disease.

Bones contain cells called osteoblasts and osteoclasts. Osteoclasts break down old bone tissue in a process called ‘resorption’, allowing it to be replaced with new healthy bone made by osteoblasts. Osteoporosis can result when the breakdown of the old bone occurs at a rate faster than formation of the new bone. Cellular senescence of osteoblasts, reducing their efficiency, might be a reason underlying this imbalance.

A gene called Men1 is linked to a genetic condition known as MEN1, causing benign tumors and associated with both cellular senescence and the development of osteoporosis early in life. The team investigated the role of Men1 in age-related osteoporosis and found that elderly mice showed both reduced levels of Men1 and increased activity of senescence-related genes in osteoblasts.

They then generated a mouse model where Men1 could be inactivated specifically in osteoblasts. The bones of these mice resembled the fragile bones seen in elderly humans. “The osteoblasts showed reduced bone formation activity, and accelerated cellular senescence through a pathway called mTORC1,” explains lead author Yuichiro Ukon, “while the numbers of osteoclasts were increased, increasing bone resorption.”

Inactivation of Men1 thus upset the balance between bone breakdown and formation, leading to the development of osteoporosis.

This new mouse model is particularly important because most studies of osteoporosis use elderly mice to mimic the human symptoms. However, natural aging involves multiple factors that influence the onset of osteoporosis, including reduced activity with increasing age and menopause-related hormonal changes.

“This model is the first time that the cellular senescence underlying osteoporosis has been modeled without the confounding factors present in elderly mice,” explains corresponding author Takashi Kaito, “and is therefore a key step forward in our understanding of the biological mechanisms behind this disease.”

The team also showed that the use of a drug called metformin, known to suppress the mTORC1 cellular senescence pathway, was able to suppress this senescence in osteoblast cells in vitro, and to partially restore the bone structure in Men1-deficient mice, indicating the potential effectiveness of osteoporosis treatments targeting cellular senescence.

This study is therefore highly significant in advancing our understanding of osteoporosis and potential treatments, as well as identifying biomarkers of the disease for evaluating the efficiency of prospective therapies. The mice developed here also provide a novel model of osteoporosis, which is key for ongoing research. Because cellular senescence has been linked to other age-related diseases and cancers, this work may provide insights into many other diseases.

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