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Organs Age At Different Rates According To A New Study

A study using animals suggests ageing is not a gradual decline of the entire body all at once, but a more disordered process with some organs ageing faster than others. How each individual organ ages depends on its cellular proteins and its physiological function in the body, new research from the Salk Institute for Biological Studies proposes.

“Ageing is associated with the decline of protein, cell, and organ function,” wrote the authors in their study. “We identify 468 differences in protein abundance between young and old animals.”

Ageing, in clinical terms, is a progressive deterioration of organ function as the cells and proteins within organs decline. Meanwhile, the activity levels of genes decrease as animals age, past studies have shown, with most genes showing similar changes across all of the organs. However, a recent study using state of the art technologies on mice tissue concluded the vast majority of proteins remain unchanged in number with age. These recent findings made the issue of age more confusing.

How exactly does ageing affect proteins, then, if it doesn’t decrease their numbers? the scientists wondered. Do age-related changes differ from organ to organ?


Co-first authors of the study, Dr. Brandon Toyama of the Salk Institute and Dr. Alessandro Ori of the European Molecular Biology Laboratory combined genomics and proteomics in their examination of young and old rats. By focusing on both genes and proteins at once, these two researchers and their colleagues were better able to analyse cellular changes in the animals’ livers and brains. What did they discover?

First, they were able to identify 468 differences in protein abundance between the younger and older animals. Second, they observed another set of 130 proteins showing age-related differences in terms of their location within cells, their phosphorylation state, or some other characteristic that would affect either the activity level or function of proteins.

Essentially, then, these discoveries expanded the list of proteins modified by age.

The scientists most dramatic finding? Most of the age-related differences in proteins could be found in just one organ or another for example the brain ageing faster than the liver. In fact, a larger proportion of proteins in the brain were affected by ageing compared to the liver. The reason why, the researchers theorized, is because cells in each of these organs function uniquely. Throughout adulthood, for instance, cells in the liver are frequently replaced. By contrast, neurons in the brain are non-dividing and must survive for the entire lifetime. And so they feel the effects of ageing most.

Based on their new findings, the researchers define ageing as an organ-specific deterioration of the cellular proteome. Going forward, they plan to study differences between individuals, nevertheless, the researchers believe this current work provides “a rich data resource to stimulate further studies of ageing.”

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1 in 3 People In The UK Will Develop Dementia Unless Changes Are Made

1 in 3 people born in the UK today will develop the disease in their lifetime unless action is taken. This is according to a new report commissioned by Alzheimer’s Research UK. There are currently 46.8 million people worldwide living with dementia, according to Alzheimer’s Disease International, and this number is expected to increase to 131.5 million by the year 2050 – particularly in developing countries.

Alzheimer’s disease is the most common form of dementia, affecting around 5.3 million people in America alone. Echoing increasing dementia rates around the globe, the number of people with Alzheimer’s in the USA is expected to almost triple to 15.8 million by the year 2050. Since age is the largest risk factor for dementia – with the condition most common among individuals aged 65 and older – rising dementia rates have been attributed to ageing populations and increases in life expectancy around the world.

This latest report – conducted by the UK’s Office of Health Economics (OHE) – set out to estimate how many people born in the UK this year are likely to develop dementia in their lifetime if no additional efforts are made to combat the condition. The results revealed that 32% of people born in the UK in 2015 – around 1 in 3 – will develop dementia in their lifetime. Calculating the numbers by gender, the report estimated that 27% of men and 37% of women born this year will develop dementia in their lifetime


According to Dr. Matthew Norton, head of policy at Alzheimer’s Research UK, these latest figures represent a “stark reality” that as people are living longer, dementia prevalence is rising, highlighting the need for greater efforts to tackle the disease. He points to previous research commissioned by Alzheimer’s Research UK that suggests the number of dementia cases could be reduced by a third if onset of the condition could be delayed by 5 years.

However, experts around the globe claim lack of funding for dementia research is one of the greatest barriers to prevention and treatment strategies for the condition.

“Dementia is the biggest health and social care challenge of our generation, but research into the condition has been hugely underfunded. This lack of funding has hampered progress and also restricted the number of scientists and clinicians working in the dementia field,” James Pickett, head of research at the UK’s Alzheimer’s Society, told Medical News Today in a Spotlight last year.

The funding figures back up Pickett’s statement. Last year, cancer received more than $5.3 billion in funding from the US National Institutes of Health (NIH). In comparison, Alzheimer’s only received $562 million.

According to Dr. Norton, this latest report emphasizes the need for greater investment in dementia research: “It’s wonderful news that each generation is living longer than the last, but it’s important to ensure that people can enjoy these extra years in good health. Dementia is our greatest medical challenge and if we are to beat it, we must invest in research to find new treatments and preventions. […] Research has the power to transform lives, and our actions now will help determine the future for children born today.”

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Scientists develop a protein patch to repair damaged hearts

Researchers have developed a “protein patch” that they say reversed damage to mouse and pig hearts caused by the onset of a heart attack. The new creation could be set to enter human clinical trials in 2017.  Prof. Pilar Ruiz-Lozano, of Stanford University, CA, and colleagues publish the details of their creation in the journal Nature.

During a heart attack, or myocardial infarction, heart muscle cells – knowns as cardiomyocytes – suffer damage and die due to lack of oxygen from reduced blood flow. In adult mammals, cardiomyocytes are unable to fully regenerate following heart attack, and as a result, the heart muscle forms scar tissue attempting to heal.

At present, there is no treatment to effectively reverse damage caused by heart attack – a condition that affects around 735,000 Americans every year. Depending on the severity, such damage may lead to further complications, including arrhythmias – abnormal heart rhythms – and heart failure.

In their study, Prof. Ruiz-Lozano and colleagues set out to develop a treatment that addresses the inability of cardiomyocytes to regenerate. Past studies in zebrafish, whose heart cells have the ability to regenerate, have revealed that the epicardium – the inner layer of the pericardium, which lines the wall of the heart muscles – plays a role in the regeneration of cardiomyocytes.

“We wanted to know what in the epicardium stimulates the myocardium, the muscle of the heart, to regenerate,” says Prof. Ruiz-Lozano. By analyzing the epicardial cells of healthy mammalian hearts, the team found that these cells triggered replication of cardiomyocytes. The team used mass spectrometry to analyze more than 300 proteins produced by epicardial cells, in an attempt to identify a single compound that may be responsible for cardiomyocyte regeneration.

Applying high throughout technology to the shortlisted candidates, the team identified a natural protein called Follistatin-like 1 (FSTL1) in epicardial tissue that stimulates cardiomyocytes to replicate. The team found, however, that after a heart attack, this protein diminishes in the epicardium.

The team then came up with an idea to turn their findings into a therapeutic strategy for treating heart attack. They created a patch made of acellular collagen that simulates fetal epicardial tissue and is embedded with FSTL1. The patch and the FSTL1 protein is slowly absorbed when applied to a damaged heart.

On testing the patch on the hearts of pigs and mice that had been damaged by heart attack, the team found it began to trigger regeneration of existing heart muscle cells and growth of new blood vessels within 4 weeks. This improved the overall heart function of the animals, as well as their survival – even when the patch was applied a week after heart attack.

“Many [of the animals] were so sick prior to getting the patch that they would have been candidates for heart transplantation,” notes Prof. Ruiz-Lozano.

Study co-author Mark Mercola, professor of bioengineering at UCSD, says the team is “excited” by the findings, stating that the patch is “clinically viable” and “clinically attractive.” What is more, because the patch is acellular – meaning it contains no cells – a patient would not need to use immunosuppressive medication.

Prof. Ruiz-Lozano believes the findings pave the way for a “completely revolutionary” treatment for heart attack patients, and the team hopes the patch will enter human clinical trials within the next 2 years.