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Tag Archives: Hallmarks
Study Traces Shared and Unique Cellular Hallmarks Found in 6 Neurodegenerative Diseases
Summary: Multiple neurodegenerative disorders harbor similar fundamental dysfunctional cellular processes.
Source: University of Arizona
A perplexing range of neurodegenerative diseases are known to attack distinct regions of the brain, causing severe cognitive and motor deficit. The combined impact of these (generally fatal) diseases has inflicted a devastating toll on society.
New insights suggest many of these afflictions have their origin in a constellation of common processes, which play out in different ways as each disease develops.
In a study appearing in the current issue of Alzheimer’s & Dementia: The Journal of the Alzheimer’ Association, corresponding author Carol Huseby of Arizona State University and her colleagues look at cellular alterations in six distinct neurodegenerative diseases: amyotrophic lateral sclerosis or Lou Gehrig’s disease, Alzheimer’s disease, Friedreich’s ataxia, frontotemporal dementia, Huntington’s disease and Parkinson’s disease.Carol Huseby is a researcher with the ASU-Banner Neurodegenerative Disease Research Center.
The study uses an innovative approach, which includes the machine learning analysis of RNA found in whole blood. By comparing multiple diseases, researchers can identify which RNA markers occur across several neurodegenerative diseases and which are unique to each disease.
“It appears that multiple neurodegenerative diseases harbor similar fundamental dysfunctional cellular processes,” says Huseby, a researcher with the ASU-Banner Neurodegenerative Disease Research Center.
“Differences between diseases may be key to discovering regional cell-type vulnerabilities and therapeutic targets for each disease.”
The blood samples used for the study were derived from a publicly available data set known as the Gene Expression Omnibus. Each of the six neurodegenerative diseases were probed. As the machine learning algorithm combed through thousands of genes, it assembled sets of RNA transcripts that optimally classified each disease, comparing the data with RNA samples from healthy patient blood.
The selected RNA transcripts reveal eight common themes across the six neurodegenerative diseases: transcription regulation, degranulation (a process involved in inflammation), immune response, protein synthesis, cell death or apoptosis, cytoskeletal components, ubiquitylation/proteasome (involved in protein degradation) and mitochondrial complexes (which oversee energy usage in cells). The eight cellular dysfunctions uncovered are associated with identifiable pathologies in the brain characteristic of each disease.
The study also identified uncommon transcripts for each disease, which may represent unexplored disease pathways. Such disease-specific outliers may be explored as a potential source of diagnostic biomarkers.
For example, while synaptic loss was a common feature in all six of the diseases analyzed, transcripts related to a phenomenon known as spliceosome regulation were only detected in the case of Alzheimer’s disease. (The spliceosome is a protein complex found in the cell nucleus, essential for proper cell function. Defective splicing of RNA is associated with disease.)
The investigation of blood biomarkers for neurodegenerative diseases, coupled with powerful statistical methods using artificial intelligence, has opened a new window on these serious afflictions. Blood can be easily sampled in living patients at all stages of health and disease, providing a powerful new tool for early diagnosis.
According to the United Nations, when all neurodegenerative diseases are considered, the global death toll may top a staggering 1 billion people. The course of many such diseases is protracted and pitiless, causing not only grave suffering to patients but a massive economic burden on health care systems.
New methods of early diagnosis, improved treatments and possible methods of prevention are vitally needed.
Most neurodegenerative diseases, however, have been tricky to accurately diagnose and stubbornly resistant to treatment, including Alzheimer’s disease (AD), the leading cause of dementia.
While genetic factors do play a role in the development of AD, most cases are regarded as sporadic, meaning the underlying causes are unclear.
This is also the case with three other diseases highlighted in the study: frontotemporal dementia, ALS and Parkinson’s disease. Huntington’s disease and Friedreich’s ataxia appear to be genetically determined and are said to be familial.
Signposts of neurodegeneration are detectable in both the central nervous and peripheral vascular systems. The diseases may also migrate from their point of origin to distant brain regions, where they inflict most of their damage.
The study describes RNA clusters or trees selected by the machine learning process, which uncovers patterns of gene expression common to the six neurodegenerative diseases explored in the study as well as expression profiles that are distinct and disease dependent.
Thousands of such trees are created and statistically compared by the machine learning algorithm, to pick out groupings of 20 transcripts that most closely align with known disease pathways in the diseases under study.
The findings offer clues about common cellular features that may play a role in jump-starting processes of neurodegeneration. The study also raises puzzling questions about how distinct disease forms ultimately develop from these common elements.
From the RNA transcripts extracted from blood, some 10,000 genes are expressed. The machine learning algorithm, known as Random Forest, categorizes the data and compares results with gene expression profiles known to be associated with disease-linked biological pathways.
Screening of whole blood and examination of the complete RNA profile can overcome the limitations of many other forms of testing, which are often less comprehensive as well as expensive, highly invasive and labor intensive.
See also
Diagnosis through whole blood, in contrast, can be carried out at low cost virtually anywhere in the world. Blood results can be tracked over time, providing a valuable window on disease progression. Research of this kind may also encourage new modes of treatment.
The results suggest a tantalizing possibility: Transcriptional changes shared by multiple disease types may provide the initial seeds that later develop into each of the distinct brain afflictions. The mechanisms responsible for these common factors germinating to produce diverse diseases and symptomologies, attacking different regions of the brain, remain a central puzzle to be solved.
Future research will explore transcriptional impacts on neurons in addition to blood cells as well as the underlying mechanisms that set the stage for neurodegenerative diseases to develop and evolve their distinct pathologies.
About this neurology and genetics research news
Author: Press Office
Source: University of Arizona
Contact: Press Office – University of Arizona
Image: The image is credited to Shireen Dooling
Original Research: Closed access.
“Blood RNA transcripts reveal similar and differential alterations in fundamental cellular processes in Alzheimer’s disease and other neurodegenerative diseases” by Carol J. Huseby et al. Alzheimer’s & Dementia
Abstract
Blood RNA transcripts reveal similar and differential alterations in fundamental cellular processes in Alzheimer’s disease and other neurodegenerative diseases
Background
Dysfunctional processes in Alzheimer’s disease and other neurodegenerative diseases lead to neural degeneration in the central and peripheral nervous system. Research demonstrates that neurodegeneration of any kind is a systemic disease that may even begin outside of the region vulnerable to the disease. Neurodegenerative diseases are defined by the vulnerabilities and pathology occurring in the regions affected.
Method
A random forest machine learning analysis on whole blood transcriptomes from six neurodegenerative diseases generated unbiased disease-classifying RNA transcripts subsequently subjected to pathway analysis.
Results
We report that transcripts of the blood transcriptome selected for each of the neurodegenerative diseases represent fundamental biological cell processes including transcription regulation, degranulation, immune response, protein synthesis, apoptosis, cytoskeletal components, ubiquitylation/proteasome, and mitochondrial complexes that are also affected in the brain and reveal common themes across six neurodegenerative diseases.
Conclusion
Neurodegenerative diseases share common dysfunctions in fundamental cellular processes. Identifying regional vulnerabilities will reveal unique disease mechanisms.
Dolphins show hallmarks of Alzheimer’s, study suggests
London
CNN
—
The brains of three species of dolphin found stranded along the Scottish coast have shown the hallmarks of Alzheimer’s disease, according to new research, providing greater insight into the disease in species other than humans.
The findings may also provide a possible answer to unexplained strandings of dolphins along the coast, researchers said.
Alzheimer’s disease is a common neurodegenerative disorder that mostly affects older humans, with symptoms such as memory loss, forgetfulness and confusion.
According to a study published December 13 in the European Journal of Neuroscience, researchers in Scotland conducted postmortem studies on the brains of 22 odontocetes, or toothed whales, making their findings more detailed compared with others, the authors said.
“It’s more in depth and breadth as it looks at larger numbers of animals from several different species of cetaceans known to be aged for the species (older in age),” Mark Dagleish, coauthor and a senior clinician in anatomic pathology from the University of Glasgow, told CNN on Tuesday.
The study looked at specimens from five species: Risso’s dolphins, long-finned pilot whales, white-beaked dolphins, harbour porpoises and bottlenose dolphins. Of the 22 studied, 18 were aged specimens.
“Critically, (it) examined the whole brains to provide lesion (abnormality) profiles using more markers of Alzheimer’s disease,” Dagleish added, with the same techniques used for human tissues.
Findings showed that three aged dolphins — a long-finned pilot whale, a white-beaked dolphin and a bottlenose dolphin — presented brain changes, or lesions, associated with Alzheimer’s disease in humans.
Tara Spires-Jones, another study coauthor, said in a statement this week that researchers “were fascinated to see brain changes in aged dolphins similar to those in human (aging) and Alzheimer’s disease.”
“Whether these pathological changes contribute to these animals stranding is an interesting and important question for future work,” said Spires-Jones, the personal chair of neurodegeneration at the University of Edinburgh’s Deanery of Biomedical Sciences.
The researchers found that the specimens had accumulated phospho-tau proteins and glial cells, and had formed amyloid-beta plaques, the clumping of a protein found in brains of people with Alzheimer’s disease. The distribution of these lesions was comparable to the brain regions in humans with Alzheimer’s, according to the research paper.
Dagleish said the findings are “the closest anyone has been able to show that any animals develop the Alzheimer’s disease-associated lesions spontaneously,” which had been thought only to develop in humans.
Odontocetes are regularly stranded on UK coasts in groups, which the study authors said may support the “sick-leader” theory of when the group follows an aged leader into shallow waters, potentially as a result of the leader’s confusion.
The similar neuropathology of the aged dolphins and humans with Alzheimer’s suggests that the marine mammals have a susceptibility to the disease, but Dagleish said that a diagnosis can only be made if there are cognitive deficits. These are typically found using cognitive impairment assessments — impossible with postmortem studies.
Is it Covid, flu or RSV? A few hallmarks can help distinguish between the illnesses
Covid, flu and respiratory syncytial virus (RSV) are together driving a national wave of respiratory illnesses.
Around 76% of U.S. hospital inpatient beds are full, according to data from the Department of Health and Human Services. Pediatric beds are at a similar level, though six states have 90% or more of their pediatric beds full, according to an NBC News analysis of HHS data.
Covid, flu and RSV can be difficult to distinguish, since they share many common symptoms. But it’s useful to know which virus you have, since that determines the treatments you should receive and how long you should isolate.
Certain hallmarks — either symptoms or how the illness progresses — can help differentiate each virus. Here are five factors to consider.
Some symptoms are unique to particular viruses
A runny nose, cough, congestion or sore throat can arise because of any of the three viruses or a common cold. But a loss of taste and smell is more commonly associated with Covid than with flu or RSV. And wheezing is often a tell-tale sign of a serious RSV infection, usually found in kids or older adults.
The only way to know for certain, though, is to get tested.
“I don’t think anybody would ever go, ‘Hey, listen, I think you have a virus based on your symptoms,’ and feel confident to say what virus that is,” said Dr. Frank Esper, a pediatric infectious disease specialist at Cleveland Clinic.
Are symptoms coming on gradually or all of a sudden?
Flu symptoms tend to develop more suddenly than those of Covid or RSV.
“Flu classically comes on with an abrupt fever first that happens pretty quickly. That’s somewhat contrasted by RSV and Covid, where we think of a slow escalation in symptoms,” said Dr. Scott Roberts, a Yale Medicine infectious disease specialist.
How long has it been since exposure?
The illnesses have different incubation periods — the time between exposure and symptoms. On average, flu symptoms tend to develop two days after exposure to the virus, whereas RSV symptoms tend to take around four to six days to appear, and Covid’s typical incubation is three to four days for the omicron variant.
“If I go to a party and I get symptoms the next day, it’s probably flu because that can be as short as 24 hours’ incubation period,” Roberts said.
Age makes a big difference in a disease’s symptoms and severity
RSV is unlikely to make a healthy adult feel very sick, whereas Covid and flu certainly can.
“In general, if you’re a young healthy adult or you’re not in an extreme of age, and you get pretty severe illness, it’s probably not RSV,” Roberts said.
The groups most vulnerable to severe RSV infections are babies, children with lung diseases, adults ages 65 and up and people with weakened immune systems.
Symptoms can also look different depending on your age and immune status. Many kids are encountering respiratory viruses for the first time this year as they return to regular schooling and socializing, so their bodies may have a harder time clearing the infection, which can lead to more wide-ranging symptoms.
According to Esper, almost a fourth of children have gastrointestinal symptoms (like diarrhea, stomach pain or vomiting) from viral infections. That’s less common in adults with seasonal flu or RSV.
People with weakened immune systems, meanwhile, are more likely to develop severe symptoms or pneumonia from any of the three viruses.
Consider which virus is circulating the most in your community
Disease experts anticipate that Covid cases will climb over the holidays as more people travel and gather indoors. Average daily cases reported to the Centers for Disease Control and Prevention have already risen nearly 11% over the last two weeks, according to NBC News’ tally.
But it’s difficult to determine local Covid transmission levels, since many people use at-home tests. RSV and flu tests, by contrast, are performed at a doctor’s office or ordered via prescription.
RSV infections seem to have passed their peak nationally. Although the CDC does not keep a national count of RSV cases, the number of positive weekly tests fell from more than 17,000 in the week ending Nov. 5 to around 9,000 in the week ending on Saturday.
By contrast, flu cases are skyrocketing. The national share of influenza tests that came back positive rose from around 8% in the week ending Oct. 30 to nearly 15% in the week ending Nov. 13. Flu hospitalizations are the highest they’ve been at this time of year in more than a decade.
Esper said he expects the Cleveland Clinic to be “swimming in flu” two weeks from now.
The picture varies by region, however. In the Northeast, Roberts said, “we saw RSV surge over the last one to two months and it’s actually plateaued — which is great news — and then flu, only the past few weeks we’re seeing an exponential rise.”
“The Southeast U.S. — Georgia, Alabama, Mississippi — they saw kind of the opposite. They saw initially a surge in flu, and then now you’re seeing RSV start to catch up,” he added.
Available treatments and vaccines
Unlike Covid and the flu, there are no vaccines or universally prescribed treatments for RSV.
“RSV scares me the most, probably, because you can’t do anything about it and so many young kids haven’t seen it. We’re really seeing record surges in our pediatric hospitals,” Roberts said.
To reduce the length of flu symptoms, though, doctors usually prescribe Tamiflu or one of three other approved treatments. For some people with Covid, doctors can prescribe Paxlovid.
Dr. Ashish Jha, the White House Covid-19 Response Coordinator, emphasized the benefits of getting flu shots and Covid boosters.
“In this moment where we have a lot of flu, still have a decent amount of RSV, still got a good amount of Covid, the single most important thing people need to do is go get vaccinated,” Jha said at a Tuesday briefing. “It keeps you out of the hospital.”
Fecal Transplants Reverse Hallmarks of Aging in the Gut, Eyes, and Brain
In an experiment on mice, transplanting fecal microbiota from young into old reversed hallmarks of aging in the gut, eyes, and brain
In the quest for eternal youth, poo transplants may seem like an unlikely way to reverse the aging process.
However, scientists at the Quadram Institute and the University of East Anglia have provided evidence, from research in mice, that transplanting fecal microbiota from young into old mice can reverse the hallmarks of aging in the gut, eyes, and brain.
In the reverse experiment, microbes from aged mice induced inflammation in the brain of young recipients and depleted a key protein required for normal vision.
These findings show that gut microbes play a role in regulating some of the detrimental effects of aging and open up the possibility of gut microbe-based therapies to combat the decline in later life.
Prof Simon Carding, from UEA’s Norwich Medical School and head of the Gut Microbes and Health Research Programme at the Quadram Institute, said: “This ground-breaking study provides tantalizing evidence for the direct involvement of gut microbes in aging and the functional decline of brain function and vision and offers a potential solution in the form of gut microbe replacement therapy.”
It has been known for some time that the population of microbes that we carry around in our gut, collectively called the gut microbiota, is linked to health. Most diseases are associated with changes in the types and behavior of bacteria, viruses, fungi, and other microbes in an individual’s gut.
Some of these changes in microbiota composition happen as we age, adversely affecting metabolism and immunity, and this has been associated with age-related disorders including inflammatory bowel diseases, along with cardiovascular, autoimmune, metabolic, and neurodegenerative disorders.
To better understand the effects of these changes in the microbiota in old age, scientists from the Quadram Institute transferred the gut microbes from aged mice into healthy young mice, and vice versa. They then looked at how this affected inflammatory hallmarks of aging in the gut, brain and eye, which suffer from declining function in later life.
The study, published in the journal Microbiome, found that the microbiota from old donors led to loss of integrity of the lining of the gut, allowing bacterial products to cross into the circulation, which results in triggering the immune system and inflammation in the brain and eyes.
Age-related chronic inflammation, known as inflammaging, has been associated with the activation of specific immune cells found in brain. These cells were also over-activated in the young mice who received aged microbiome transplants.
In the eye, the team also found specific proteins associated with retinal degeneration were elevated in the young mice receiving microbiota from old donors.
In old mice, these detrimental changes in the gut, eye and brain could be reversed by transplanting the gut microbiota from young mice.
In ongoing studies, the team is now working to understand how long these positive effects can last, and to identify the beneficial components of the young donor microbiota and how they impact on organs distant from the gut.
The microbiota of young mice, and the old mice who received young microbiota transplants were enriched in beneficial bacteria that have previously been associated with good health in both mice and humans.
The researchers have also analyzed the products which these bacteria produce by breaking down elements of our diet. This has uncovered significant shifts in particular lipids (fats) and vitamin metabolism, which may be linked to the changes seen in inflammatory cells in the eye and brain.
Similar pathways exist in humans, and the human gut microbiota also changes significantly in later life, but the researchers caution about extrapolating their results directly to humans until similar studies in elderly humans can be performed.
A new facility for Microbiota Replacement Therapy (MRT), also known as Faecal Microbiota Transplantation (FMT) is being built in the Quadram Institute that will facilitate such trials, as well as other trials for microbiota-related conditions.
Lead author of the study, Dr. Aimee Parker from the Quadram Institute said: “We were excited to find that by changing the gut microbiota of elderly individuals, we could rescue indicators of age-associated decline commonly seen in degenerative conditions of the eye and brain.
“Our results provide more evidence of the important links between microbes in the gut and healthy aging of tissues and organs around the body. We hope that our findings will contribute ultimately to understanding how we can manipulate our diet and our gut bacteria to maximize good health in later life.”
The research was funded by the Biotechnology and Biological Sciences Research Council, part of UK Research and Innovation.
‘Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain’ is published in the journal Microbiome.
Reference: “Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain” by Aimée Parker, Stefano Romano, Rebecca Ansorge, Asmaa Aboelnour, Gwenaelle Le Gall, George M. Savva, Matthew G. Pontifex, Andrea Telatin, David Baker, Emily Jones, David Vauzour, Steven Rudder, L. Ashley Blackshaw, Glen Jeffery and Simon R. Carding, 29 April 2022, Microbiome.
DOI: 10.1186/s40168-022-01243-w
Fecal Transplants Reverse Hallmarks of Aging
Summary: Transplanting fecal microbiota from young mice to older mice reversed hallmark signs of aging in the gut, brains, and eyes. Transplanting the fecal microbiota from old to young mice had the reverse effect, inducing inflammation in the brain and depleting a key protein associated with healthy vision.
Source: University of East Anglia
In the search for eternal youth, poo transplants may seem like an unlikely way to reverse the aging process.
However, scientists at the Quadram Institute and the University of East Anglia have provided evidence, from research in mice, that transplanting fecal microbiota from young into old mice can reverse hallmarks of aging in the gut, eyes, and brain.
In the reverse experiment, microbes from aged mice induced inflammation in the brain of young recipients and depleted a key protein required for normal vision.
These findings show that gut microbes play a role in the regulating some of the detrimental effects of aging and open up the possibility of gut microbe-based therapies to combat decline in later life.
Prof Simon Carding, from UEA’s Norwich Medical School and head of the Gut Microbes and Health Research Program at the Quadram Institute, said: “This ground-breaking study provides tantalizing evidence for the direct involvement of gut microbes in aging and the functional decline of brain function and vision and offers a potential solution in the form of gut microbe replacement therapy.”
It has been known for some time that the population of microbes that we carry around in our gut, collectively called the gut microbiota, is linked to health. Most diseases are associated with changes in the types and behavior of bacteria, viruses, fungi and other microbes in an individual’s gut.
Some of these changes in microbiota composition happen as we age, adversely affecting metabolism and immunity, and this has been associated with age-related disorders including inflammatory bowel diseases, along with cardiovascular, autoimmune, metabolic and neurodegenerative disorders.
To better understand the effects of these changes in the microbiota in old age, scientists from the Quadram Institute transferred the gut microbes from aged mice into healthy young mice, and vice versa. They then looked at how this affected inflammatory hallmarks of aging in the gut, brain and eye, which suffer from declining function in later life.
The study, published in the journal Microbiome, found that the microbiota from old donors led to loss of integrity of the lining of the gut, allowing bacterial products to cross into the circulation, which results in triggering the immune system and inflammation in the brain and eyes.
Age-related chronic inflammation, known as inflammaging, has been associated with the activation of specific immune cells found in brain. These cells were also over-activated in the young mice who received aged microbiome transplants.
In the eye, the team also found specific proteins associated with retinal degeneration were elevated in the young mice receiving microbiota from old donors.
In old mice, these detrimental changes in the gut, eye and brain could be reversed by transplanting the gut microbiota from young mice.
In ongoing studies, the team are now working to understand how long these positive effects can last, and to identify the beneficial components of the young donor microbiota and how they impact on organs distant from the gut.
The microbiota of young mice, and the old mice who received young microbiota transplants were enriched in beneficial bacteria that have previously been associated with good health in both mice and humans.
The researchers have also analyzed the products which these bacteria produce by breaking down elements of our diet. This has uncovered significant shifts in particular lipids (fats) and vitamin metabolism, which may be linked to the changes seen in inflammatory cells in the eye and brain.
Similar pathways exist in humans, and the human gut microbiota also changes significantly in later life, but the researchers caution about extrapolating their results directly to humans until similar studies in elderly humans can be performed.
A new facility for Microbiota Replacement Therapy (MRT), also known as Fecal Microbiota Transplantation (FMT) is being built in the Quadram Institute that will facilitate such trials, as well as other trials for microbiota-related conditions.
Lead author of the study, Dr. Aimee Parker from the Quadram Institute said: “We were excited to find that by changing the gut microbiota of elderly individuals, we could rescue indicators of age-associated decline commonly seen in degenerative conditions of the eye and brain.
See also
“Our results provide more evidence of the important links between microbes in the gut and healthy aging of tissues and organs around the body. We hope that our findings will contribute ultimately to understanding how we can manipulate our diet and our gut bacteria to maximize good health in later life.”
About this microbiome and aging research news
Author: Press Office
Source: University of East Anglia
Contact: Press Office – University of East Anglia
Image: The image is in the public domain
Original Research: Closed access.
“Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain” by Aimée Parker et al. Microbiome
Abstract
Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain
Background
Altered intestinal microbiota composition in later life is associated with inflammaging, declining tissue function, and increased susceptibility to age-associated chronic diseases, including neurodegenerative dementias. Here, we tested the hypothesis that manipulating the intestinal microbiota influences the development of major comorbidities associated with aging and, in particular, inflammation affecting the brain and retina.
Methods
Using fecal microbiota transplantation, we exchanged the intestinal microbiota of young (3 months), old (18 months), and aged (24 months) mice. Whole metagenomic shotgun sequencing and metabolomics were used to develop a custom analysis workflow, to analyze the changes in gut microbiota composition and metabolic potential. Effects of age and microbiota transfer on the gut barrier, retina, and brain were assessed using protein assays, immunohistology, and behavioral testing.
Results
We show that microbiota composition profiles and key species enriched in young or aged mice are successfully transferred by FMT between young and aged mice and that FMT modulates resulting metabolic pathway profiles. The transfer of aged donor microbiota into young mice accelerates age-associated central nervous system (CNS) inflammation, retinal inflammation, and cytokine signaling and promotes loss of key functional protein in the eye, effects which are coincident with increased intestinal barrier permeability. Conversely, these detrimental effects can be reversed by the transfer of young donor microbiota.
Conclusions
These findings demonstrate that the aging gut microbiota drives detrimental changes in the gut–brain and gut–retina axes suggesting that microbial modulation may be of therapeutic benefit in preventing inflammation-related tissue decline in later life.