Tag: ageing

Categories : AgeingTags :

Inability to Dispose of Old Cells Leads to Macular Degeneration

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Researchers have discovered that failing to dispose of old photoreceptor cells leads to age-related macular degeneration.

The estimated number of people worldwide with age-related macular degeneration in 2020 was 196 million, increasing to 288 million in 2040. Though more than 50 genes are associated with the condition, the precise mechanism is unknown. Most people have a form of the condition, for which there are no known effective treatments.

In order to develop new therapies to treat the disease, University of Maryland School of Medicine (UMSOM) researchers are starting to understand what goes wrong in the disease. Using human and mice tissue, researchers showed that the process which removes the eye’s old, damaged light sensors is disrupted in macular degeneration.

Previously, the lead researcher had found out that many families with hearing disorders had genetic mutations in the gene for the CIB2 protein, and later work also showed that CIB2 was needed for vision in a large human family, as well as in zebrafish. Now, in this latest study, his team built on that previous work to dissect the intricate cell mechanisms behind retinal degeneration.

The team compared healthy mouse eyes to those from a mouse with the CIB2 protein genetically deleted. These CIB2 mutant mice were not disposing of their old light sensor proteins, called photoreceptors, like healthy mouse eyes did.  

“Photoreceptors continue growing in tiny columns in the eye, but over time, light damages the photoreceptors. To combat this, support cells in the eye slowly munch on the old, damaged photoreceptors, keeping the columns the correct length,” explained first author Saumil Sethna, PhD, at the University of Maryland School of Medicine. “If the photoreceptors are not removed, or if the process is backed up due to slow digestion by the support cells, like in the CIB2 mutant mice, the undigested material builds up over time, which may contribute to blindness.”

The researchers then identified several components in this photoreceptor recycling process, including a group of proteins collectively called mTORC1, which is involved in many human diseases, including cancer, obesity, and epilepsy.

Since mTORC1 (part of a family called mTOR) is a decision-maker for many cellular functions including cleaning up cellular debris, the researchers examined mTORC1’s activity in the CIB2 mutant mice and saw that it was overactive. mTORC1 was also found to be overactive in eye tissue of people with a form of age-related macular degeneration. The findings therefore indicate that drugs against mTORC1 may be effective treatments for the most common type of age-related macular degeneration, according to the researcher.
“Researchers have tested many small molecules directed at mTORC1 to treat various diseases, but the problem is that mTOR is needed for so many other cell functions that there are major side-effects when you tinker with it,” said senior author Zubair M Ahmed, PhD, Professor of Otorhinolaryngology-Head & Neck Surgery and Ophthalmology at the University of Maryland School of Medicine. “In our study, we found a backdoor way to regulate mTORC1, which may bypass many of the unpleasant side-effects that normally occur with suppressing mTORC1. We think we may be able to use our new knowledge of this mechanism to develop treatments for age-related macular degeneration and other diseases as well.”

Source: University of Maryland School of Medicine

Categories : AgeingTags :

Study Confirms that Stress Turns Hair Grey – But It’s Reversible

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A new study for the first time provides quantitative evidence linking psychological stress to greying hair in people. 

Greying of hair, a phenomenon still poorly understood in humans, first starts in white individuals at 34, while black individuals only start greying around 44. While it may seem intuitive that stress can accelerate greying, the researchers were surprised to discover that hair colour can actually be restored when stress is eliminated, a finding that contrasts with a recent study in mice that suggested that stressed-induced grey hairs are permanent.

The study holds clues to understanding ageing beyond just confirming the old tale about stress and ageing, said the study’s senior author Martin Picard, PhD, associate professor of behavioral medicine (in psychiatry and neurology) at Columbia University Vagelos College of Physicians and Surgeons.  

“Understanding the mechanisms that allow ‘old’ grey hairs to return to their ‘young’ pigmented states could yield new clues about the malleability of human ageing in general and how it is influenced by stress,” Prof Picard said.

“Our data add to a growing body of evidence demonstrating that human ageing is not a linear, fixed biological process but may, at least in part, be halted or even temporarily reversed.”

Hair can help understand ageing

“Just as the rings in a tree trunk hold information about past decades in the life of a tree, our hair contains information about our biological history,” Picard said. “When hairs are still under the skin as follicles, they are subject to the influence of stress hormones and other things happening in our mind and body. Once hairs grow out of the scalp, they harden and permanently crystallise these exposures into a stable form.”

Though it has long been believed by people that psychological stress can increase grey hairs, it has remained a matter of scientific debate due to a lack of sensitive methods that can precisely correlate times of stress with hair pigmentation at a single-follicle level.

Splitting hairs to document hair pigmentation

Ayelet Rosenberg, first author on the study and a student in Picard’s laboratory, developed a new method for making high resolution images of tiny slices of human hairs to measure the extent of pigment loss — greying — in each of those slices. Each slice, about 1/20th of a millimetre wide, represents about an hour of hair growth.

“If you use your eyes to look at a hair, it will seem like it’s the same color throughout unless there is a major transition,” Picard says. “Under a high-resolution scanner, you see small, subtle variations in color, and that’s what we’re measuring.”

For the study 14 volunteers were asked to review their calendars and rate each week’s level of stress in a stress diary. Analysing individual hair samples, the researchers compared the results with each volunteer’s stress diary.

Right away, it was noticed that some grey hairs naturally regain their original color, which had never been quantitatively documented, Picard said.

When hairs were aligned with stress diaries, it revealed striking associations between stress and hair greying and, in some cases, a reversal of greying with the lifting of stress.

“There was one individual who went on vacation, and five hairs on that person’s head reverted back to dark during the vacation, synchronized in time,” Picard said.

Blame the mind-mitochondria connection

Measuring levels of different proteins in the hairs and how protein levels changed over the length of each hair, the researchers came up with a model showing that mitochondria were responsible for greying.

“We often hear that the mitochondria are the powerhouses of the cell, but that’s not the only role they play,” Picard said. “Mitochondria are actually like little antennas inside the cell that respond to a number of different signals, including psychological stress.”

The mitochondria connection between stress and hair colour is a different mechanism than found in a recent study of mice, where stress-induced greying was caused by an irreversible loss of stem cells in the hair follicle.

“Our data show that greying is reversible in people, which implicates a different mechanism,”  said co-author Ralf Paus, PhD, professor of dermatology at the University of Miami Miller School of Medicine. “Mice have very different hair follicle biology, and this may be an instance where findings in mice don’t translate well to people.”

Hair re-pigmentation possible only for some

Stress reduction is a good idea, but it won’t necessarily get rid of your grey hairs.

“Based on our mathematical modeling, we think hair needs to reach a threshold before it turns grey,” Picard said. “In middle age, when the hair is near that threshold because of biological age and other factors, stress will push it over the threshold and it transitions to grey.

“But we don’t think that reducing stress in a 70-year-old who’s been grey for years will darken their hair or increasing stress in a 10-year-old will be enough to tip their hair over the grey threshold.”

Source: Columbia University Irving Medical Center 

Journal information: Ayelet M. Rosenberg et al, Quantitative mapping of human hair greying and reversal in relation to life stress, eLife (2021). DOI: 10.7554/eLife.67437

Categories : Cardiovascular Disease NeurologyTags :

Statins not Associated With Cognitive Decline

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A new study has found that statin use in adults 65 years old or older is not associated with incident dementia, mild cognitive impairment (MCI) or decline in individual cognition domains.

Major health concerns in the elderly, cognitive decline and dementia affect about 10% of people over 60 years old. Statins are used to reduce low-density lipoprotein cholesterol, and are a fundamental treatment for prevention of primary and secondary cardiovascular disease (CVD) events. 
In 2012 the Food and Drug Administration issued a warning about cases of apparent short-term cognitive impairment with statin use, while acknowledging that the cardiovascular benefits outweigh their risks. Systematic reviews have since shown insufficient evidence on the impact of statins, and research has shown mixed results, with some showing a neurocognitive benefit of statins and others reporting a null effect.

“With statins being increasingly prescribed to older adults, their potential long-term effects on cognitive decline and dementia risk have attracted growing interest,” said lead author Zhen Zhou, PhD, Menzies Institute for Medical Research at the University of Tasmania. “The present study adds to previous research by suggesting that statin use at baseline was not associated with subsequent dementia incidence and long-term cognitive decline in older adults.”

Researchers of this study analysed data from the ASPirin in Reducing Events in the Elderly (ASPREE) trial. ASPREE was a large prospective, randomized placebo-controlled trial of daily low-dose aspirin with adults 65 or older. One of the key selection criteria of ASPREE was that participants had to have a score of 78 for the Modified Mini-Mental State Examination test, a screening test for cognitive abilities, at enrollment.

The study had 18 846 participants, grouped by their baseline statin use (31.3% of participants) versus non-statin use. The study aimed to measure outcomes including incident dementia and its subclassifications (probable Alzheimer’s disease [AD], mixed presentations); MCI and its subclassifications (MCI consistent with AD, MCI-other); changes in domain-specific cognition including global cognition, memory, language and executive function, and psychomotor speed; and in the composite of these domains.

After a median of 4.7 years of follow-up, researchers found 566 incident cases of dementia (including probable AD and mixed presentations). Compared with no statin use, statin use was not associated with risk of all-cause dementia, probable AD or mixed presentations of dementia. There were 380 incident cases of MCI found (including MCI consistent with AD and MCI-other). Compared to no statin use, statin use was not associated with risk of MCI, MCI consistent with AD or other MCI. No statistically significant difference in the change of composite cognition and any individual cognitive domains between statin users versus non-statin users was seen. However, researchers did find interaction effects between baseline cognitive ability and statin therapy for all dementia outcomes.

The researchers acknowledged several limitations, including observational study bias and lack of data on the length of prior use of statins; and the dose of statins was not recorded in the ASPREE trial, so their effects could not be fully explored. Researchers conclude the study must be interpreted with caution and will require confirmation by randomized clinical trials designed to explore the neurocognitive effects of statins in older populations.

In an accompanying editorial comment, Christie M. Ballantyne, MD, professor at Baylor College of Medicine in Houston, noted study limitations that the authors address, but agreed the findings suggest statins do not contribute to cognitive decline.

“Overall, the analysis was well done, and its main strengths are a large cohort with a battery of standardised tests that allowed the investigators to track both cognition and incidence of dementia and its subtypes over time,” Ballantyne said. “Lingering questions such as the one raised by this analysis regarding potential adverse effects of statins in individuals with mildly impaired cognition can only be answered in randomised controlled trials in the appropriate age group and population and with appropriate testing and adequate follow-up. In the meantime, practising clinicians can have confidence and share with their patients that short-term lipid lowering therapy in older individuals, including with statins, is unlikely to have a major impact on cognition.”

Source: American College of Cardiology

Categories : Ageing Immune SystemTags :

Chronic Inflammation Ages the Pituitary Gland in Mice

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Researchers have discovered that the pituitary gland in mice ages due to an age-related form of chronic inflammation — which raises the possibility of slowing or even partially repairing this process. 

The pituitary gland is a small, globular gland located underneath the brain that plays a major role in the hormonal system, explained Professor Hugo Vankelecom, a stem cell biologist from the Department of Development and Regeneration at KU Leuven. “My research group discovered that the pituitary gland ages as a result of a form of chronic inflammation that affects tissue and even the organism as a whole,” he said. “This natural process usually goes unnoticed and is referred to as ‘inflammaging’ — a contraction of inflammation and ageing. Inflammaging has previously been linked to the ageing of other organs.”

Because of the pituitary’s pivotal role in the body, its ageing may contribute to the reduction of hormonal processes and hormone levels in our body – such as in menopause.

The study also provides significant insight into the stem cells in the ageing pituitary gland. In 2012, Prof Vankelecom and colleagues showed that a prompt reaction of these stem cells to injury in the gland leads to repair of the tissue, even in adult animals.

“As a result of this new study, we now know that stem cells in the pituitary do not lose this regenerative capacity when the organism ages. In fact, the stem cells are only unable to do their job because, over time, the pituitary becomes an ‘inflammatory environment’ as a result of the chronic inflammation. But as soon as the stem cells are taken out of this environment, they show the same properties as stem cells from a young pituitary.”

Could damage be repaired?

This insight opens up a number of potential therapeutic avenues: would it be possible to reactivate the pituitary? This wouldn’t just involve slowing down hormonal ageing processes, but also repairing the damage caused by a tumour in the pituitary, for example. 

“No fewer than one in every 1000 people is faced with this kind of tumour — which causes damage to the surrounding tissue — at some point.

“The quality of life of many of these patients would be drastically improved if we could repair this damage. We may be able to do so by activating the stem cells already present — for which our present study also provides new indications — or even by transplanting cells. That said, these new treatment options are not quite around the corner just yet, as the step from fundamental research to an actual therapy can take years to complete. For the time being, our study sets out a potential direction for further research.”

The study also brings up another interesting approach: using anti-inflammatory drugs to slow down pituitary ageing or even rejuvenate an ageing pituitary. “Several studies have shown that anti-inflammatory drugs may have a positive impact on some ageing organs. No research has yet been performed on this effect in relation to the pituitary.”

From mice to humans

Since Prof Vankelecom and colleagues studied the pituitary of mice, further research is required to demonstrate whether their findings also apply to humans. Prof Vankelecom cautioned, however: “Mice have a much greater regeneration capacity than humans.

“They can repair damaged teeth, for instance, while humans have lost this ability over the course of their evolution. Regardless, there are plenty of signs suggesting that pituitary processes in mice and humans are similar, and we have recent evidence to hand that gene expression in the pituitaries of humans and mice is very similar. As such, it is highly likely that the insights we gained will equally apply to humans.”

Source: KU Leuven

Journal information: Vennekens, A., et al. (2021) Interleukin-6 is an activator of pituitary stem cells upon local damage, a competence quenched in the aging gland. Proceedings of the National Academy of Sciences. doi.org/10.1073/pnas.2100052118.

Categories : Ageing Neurodegenerative DiseasesTags :

Molecule Found to Play a Key Role in Brain Rejuvenation

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A new study shows that a molecule could play a key role in support cells in the brain, allowing them to repair and properly communicate.

Studies have shown that new brain cells continually formed in response to injury, physical exercise, and mental stimulation. Glial cells, and in particular oligodendrocyte progenitors, are highly responsive to external signals and injuries. They can detect changes in the nervous system and form new myelin, which forms a sheath around nerves, providing metabolic support and accurate transmission of electrical signals. However, less myelin is formed with age, and this progressive decline has been linked to the age-related cognitive and motor deficits observed in older people. Impaired myelin formation also has been reported in older individuals with neurodegenerative diseases such as Multiple Sclerosis or Alzheimer’s and identified as one of the causes of their progressive clinical deterioration.

A new study from the Neuroscience Initiative team at the Advanced Science Research Center at The Graduate Center, CUNY (CUNY ASRC) has identified a molecule called ten-eleven-translocation 1 (TET1) as a necessary component of myelin repair. shows that TET1 modifies the DNA in specific glial cells in adult brains so they can form new myelin in response to injury. The study was published in Nature Communications.

“We designed experiments to identify molecules that could affect brain rejuvenation,” said lead author Sarah Moyon, PhD, a research assistant professor with the CUNY ASRC Neuroscience Initiative. “We found that TET1 levels progressively decline in older mice, and with that, DNA can no longer be properly modified to guarantee the formation of functional myelin.”

The authors are currently exploring whether raising levels of TET1 in older mice could rejuvenate the oligodendroglial cells, restoring their regenerative functions.

Combining whole-genome sequencing bioinformatics, the authors showed that the DNA modifications induced by TET1 in young adult mice were essential to promote healthy communication among central nervous system cells and for ensuring proper function. The authors also showed that young adult mice with a genetic modification of TET1 in the myelin-forming glial cells could not produce functional myelin, and so behaved like older mice.

“This newly identified age-related decline in TET1 may account for the inability of older individuals to form new myelin,” said Patrizia Casaccia, founding director of the CUNY ASRC Neuroscience Initiative, a professor of Biology and Biochemistry at The Graduate Center, CUNY, and the study’s primary investigator. “I believe that studying the effect of aging in glial cells in normal conditions and in individuals with neurodegenerative diseases will ultimately help us design better therapeutic strategies to slow the progression of devastating diseases like multiple sclerosis and Alzheimer’s.”

The findings could also hold important implications for molecular rejuvenation of ageing brains in healthy individuals, the researchers noted. Future studies aimed at increasing TET1 levels in older mice are underway to define whether the molecule could restore new myelin formation and favour proper neuro-glial communication. The long-term goal of the team is to promote recovery of cognitive and motor functions in older people and in patients with neurodegenerative diseases.

Source: Advanced Science Research Center

Categories : AgeingTags :

Hearing Loss in Older People Can be Prevented While Young

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Based on a new model, researchers have proposed a way to prevent hearing loss in older people by addressing socioeconomic inequalities encountered while young.

The model developed by University of Manchester researchers could have an impact on the estimated 466 million people worldwide with disabling hearing loss, which mostly affects the elderly.

Published in Trends in Hearing, this is the first study examining the mechanisms and explaining the relationship between a lifetime of socioeconomic inequalities and hearing health.

Previous studies have shown that people with hearing loss are more likely to have poorer educational achievement, higher rates of unemployment and lower annual family income compared to those with other health conditions.

They are also more likely to have long-term health conditions and a higher overall disease burden than older people without hearing loss.

Lead researcher Dr Dalia Tsimpida said: “Hearing deterioration is a lifelong process but not an inevitable result of aging. Understanding this process is an essential step in addressing the global burden of hearing loss.”

Dr Tsimpida, a postdoctoral researcher at the University’s Institute for Health Policy and Organization (IHPO), added: “The key determinants of poor hearing health in the course of a life and their interdependency as described by this model is a powerful way to intervene in this major problem.

“Our focus is not simply on the age of older adults but on factors which impact on people earlier in life, which if modified could reduce hearing loss in older age.”

“This approach in hearing health can lead to the development of appropriate interventions and public health strategies that can have significant health policy and practice implications.”

Study co-author Dr Maria Panagioti said: “This model provides now a visual representation of the several modifiable factors of hearing loss in distinct life stages and their evolution over time, which is new thinking in hearing loss research.

“Given the burden of adult-onset hearing loss, such a conceptual tool for hearing health inequalities has the potential of improving the physical, mental and social wellbeing of individuals.”

Source: Medical Xpress

Journal information: Dialechti Tsimpida et al, Conceptual Model of Hearing Health Inequalities (HHI Model): A Critical Interpretive Synthesis, Trends in Hearing (2021). DOI: 10.1177/23312165211002963

Categories : AgeingTags :

Tooth Loss may Decrease the Capacity to Perform Everyday Tasks

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Older adults with more natural teeth are better able to perform everyday tasks such as cooking a meal, making a telephone call or going shopping, according to a new study. 

The study, conducted by researchers from UCL and the Tokyo Medical and Dental University, was published in the Journal of American Geriatrics Society, The researchers analysed data from 5631 adults from the English Longitudinal Study of Ageing (ELSA) with ages between 50 and 70 years old.

Previous research had established a link between tooth loss and various reductions in capacity, such as cognitive decline. However, such research could not tease out any kind of causal link: did the tooth loss cause the decline, or did the decline result in tooth loss?

In this study the research team wanted to investigate the causal effect of tooth loss on someone’s ability to carry out daily activities. After controlling for factors such as participants’ socioeconomic status and health status, they nevertheless found evidence of an independent link between tooth loss and the ability to carry out everyday tasks.

The participants in the study were asked how many natural teeth they had, with older adults usually having up to 32 natural teeth that are lost over time. Using data gathered in 2014-2015, the researchers measured how tooth loss affected people’s ability to carry out key instrumental activities of daily living (IADL). The activities included preparing a hot meal, shopping for groceries, making telephone calls, taking medications, doing work around the house or garden, or managing money.

Senior author Georgios Tsakos, professor at UCL Institute of Epidemiology and Health, explained: “We know from previous studies that tooth loss is associated with reduced functional capacity, but this study is the first to provide evidence about the causal effect of tooth loss on the instrumental activities of daily living (IADL) among older adults in England. And this effect is considerable.

“For example, older adults with 10 natural teeth are 30% more likely to have difficulties with key activities of daily living such as shopping for groceries or working around the house or garden compared to those with 20 natural teeth.

“Even after taking in factors such as participant’s education qualification, self-rated health and their parent’s education level for example, we still found a positive association between the number of natural teeth a person had and their functional ability.”

The researchers had a number of possible explanations for this relationship, noting that having more natural teeth is linked to delaying the onset of disability and death and that tooth loss can also hamper social interactions, which is also linked to poorer quality of life. Tooth loss could be linked to having a poorer diet with less nutrients, they suggested.

However the researchers cautioned that the results should be considered carefully due to the study’s complex design. Further studies are needed to investigate the causal relationship between tooth loss and functional ability.

First author, Dr Yusuke Matsuyama, at Tokyo Medical and Dental University, said: “Preventing tooth loss is important for maintaining functional capacity among older adults in England. Given the high prevalence of tooth loss, this effect is considerable and maintaining good oral health throughout the life course could be one strategy to prevent or delay loss of functional competence.

“The health gain from retaining natural teeth may not be limited to oral health outcomes but have wider relevance for promoting functional capacity and improving overall quality of life.”

Source: University College London

Journal information: Yusuke Matsuyama et al, Causal Effect of Tooth Loss on Functional Capacity in Older Adults in England: A Natural Experiment, Journal of the American Geriatrics Society (2021). DOI: 10.1111/jgs.17021

Categories : AgeingTags :

Lifestyle Interventions Reverse the DNA Methylation Ageing ‘Clock’

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The results of a clinical trial showed that appropriate diet and exercise are able, to some extent, to reverse the DNA methylation ageing ‘clock’.

Lead author Kara Fitzgerald, ND IFMCP, at The Institute for Functional Medicine, explained: “Advanced age is the largest risk factor for impaired mental and physical function and many non-communicable diseases including cancer, neurodegeneration, type 2 diabetes, and cardiovascular disease.”

Methylation clocks are based on systematic methylation changes with age. DNAmAge clock specifically demonstrates about 60% of CpG sites losing methylation with age and 40% gaining methylation.

The researchers conducted a randomised controlled clinical trial conducted among 43 healthy adult males between the ages of 50-72. The 8-week treatment programme included diet, sleep, exercise and relaxation guidance, and supplemental probiotics and phytonutrients.

Genome-wide DNA methylation analysis was conducted on saliva samples using the Illumina Methylation Epic Array and DNAmAge was calculated using the online Horvath DNAmAge clock tool.

The researchers found that the diet and lifestyle treatment resulted in a 3.23 years decrease in DNAmAge compared with controls.

With a strong trend to significance, DNAmAge of those in the treatment group decreased by an average 1.96 years by the end of the program compared to those individuals’ baseline.

Nearly a quarter of the DNAmAge CpG sites are located in glucocorticoid response elements, indicating a likely relationship between stress and accelerated ageing. Cumulative lifetime stress has been shown to be linked to accelerated ageing of the methylome.

Other findings include that PTSD contributes to accelerated methylation age; and that greater infant distress is associated with an underdeveloped, younger epigenetic age.

The researchers tentatively accepted the hypothesis that the methylation pattern, from which the DNAmAge clock is computed, is a driver of ageing, thus they expect that attempting to directly influence the DNA methylome using diet and lifestyle to set back DNAmAge should lead to a healthier, more ‘youthful’ metabolism.

The Fitzgerald Research Team concluded, “it may be that emerging ‘omics’ approaches continue to evolve our understanding of biological age prediction and reversal beyond DNA methylation alone. Integration of our future understanding of multi-omics data should therefore be considered in the future trials of candidate age-delaying interventions.”

Source: Aging

Journal information: Fitzgerald, K. N., et al. (2021) Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial. AGING-US. doi.org/10.18632/aging.202913.

Categories : Ageing PaediatricsTags :

Telomere Length May Be Set Early in Life

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Telomeres, the protective nucleotide end caps of chromosomes which shorten with every cell division, have been found by a new study to undergo great changes in length during the first years of life.

The length of telomeres is important in a number of age-related diseases and is also an important marker of biological age. When telomeres are completely shortened, cells become senescent and unable to divide any further to repair damage.

This study, one of the first to examine telomere length (TL) in childhood, found that the initial setting of TL during prenatal development and in the first years of life may determine one’s TL throughout childhood and potentially even into adulthood or older age. The study also finds that TL decreases most rapidly from birth to age 3, then remaining unchanged into the pre-puberty period, although on some occasions it was seen to lengthen.

Researchers at the Columbia Center for Children’s Environmental Health at Columbia University Mailman School of Public Health led the study, which followed 224 children from birth to age 9. Their findings were published in the journal Psychoneuroendocrinology.

The researchers discovered that a mother’s TL is predictive of newborn TL and tracks with her child’s TL through pre-adolescence. The reasons why some children have telomeres that shorten faster are unknown, though one explanation may be that telomeres are susceptible to environmental pollutants. It is also unknown why some children had telomeres that lengthened across the study period, a phenomenon seen in other studies.

“Given the importance of telomere length in cellular health and aging, it is critical to understand the dynamics of telomeres in childhood,” said senior author Julie Herbstman, PhD, director of CCCEH and associate professor of environmental health science at Columbia Mailman School. “The rapid rate of telomere attrition between birth and age 3 years may render telomeres particularly susceptible to environmental influences during this developmental window, potentially influencing life-long health and longevity.”

Researchers used polymerase chain reaction to measure TL in white blood cells isolated from cord blood and blood collected at ages 3, 5, 7, and 9, from 224 children. In a small group of mothers they also measured maternal TL at delivery.

The researchers said that further research is needed to understand the biological mechanisms behind the variance of TL shortening or lengthening rates in the first years of life, as well as modifiable environmental factors contributing to the shortening speed.

Source: Columbia Mailman School of Health

Categories : Gender Neurodegenerative DiseasesTags :

High Blood Pressure Dementia Risk Found for Women

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Differences in blood pressure’s influence on dementia risk in men and women may provide clues to help slow the rapid progress of the disease, according to new research.

In a study involving half a million people, researchers found that although the link between several mid-life cardiovascular risk factors and dementia was similar for both sexes, for blood pressure it was not. Low and high blood pressure were both shown to be associated with a greater risk of dementia in men, but for women the risk of dementia increased as blood pressure went up.

Lead author Jessica Gong said that while more research was needed to verify these findings, they may point to better ways of managing risk.

“Our results suggest a more tailored approach to treating high blood pressure could be more effective at preventing future cases of dementia,” she said.

Dementia is fast becoming a global epidemic, currently affecting an estimated 50 million people worldwide. This is projected to triple by 2050 – mainly driven by aging populations. Rates of dementia and associated deaths are both known to be higher in women than men.

In 2016 it overtook heart disease as the leading cause of death in Australian women and it is the second leading cause of death for all Australians.

With no treatment breakthroughs of any significance, the focus has therefore been on cutting the risk of developing the disease. Cardiovascular risk factors are increasingly recognised as contributors to different types of dementia.

To explore differences in major cardiovascular risk factors for dementia between the sexes, George Institute researchers accessed data from the UK Biobank, a large-scale biomedical database that recruited 502 489 dementia-free Britons 40-69 years old between 2006 and 2010.

They found that, to a similar degree in women and men, smoking , diabetes, high body fat levels, prior stroke history, and low socio-economic status were all linked to a greater risk of dementia.

But when it came to blood pressure, the relationship with dementia risk between the sexes was different. Although the reason for this wasn’t clear, the authors proposed some possible explanations.

“Biological differences between women and men may account for the sex differences we saw in the relationship between blood pressure and the risk of dementia,” said Ms Gong.

“But there may also be differences in medical treatment for hypertension. For example, women are less likely to take medication as prescribed by their healthcare provider than men and may be taking more medications and experiencing more side effects.”

While there are no effective treatments for dementia, trying to reduce the burden of the disease by encouraging healthier lifestyles is the priority, and the strongest evidence points to blood pressure management.

“Our study suggests that a more individualised approach to treating blood pressure in men compared to women may result in even greater protection against the development of dementia,” said study co-author Professor Mark Woodward.

“It also shows the importance of ensuring sufficient numbers of women and men are recruited into studies and that the data for women and men should be analysed separately,” he added.

Source: George Institute