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In the end, it will be the microbes – bacteria, viruses and fungi – that will be at the root of all diseases and aging, and More specifically from Alzheimer's disease Rudolph "Rudy" Emile Tanzi.
"The two greatest threats to healthy aging relate to infection," says Tanzi, a specialist in the disease Alzheimer's and brain at Massachusetts General Hospital (MGH) and at Harvard Medical School.When we increased the life span from 35 to 50, it was by covering the sewers, when we increased the lifespan of 50 to 75, it was with the use of antibiotics, the main life-threatening diseases of our time – Alzheimer's disease, cancer, Parkinson's disease – and guess what? The infection is now popping up in every one of them. "
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And although evidence continues to mount his theory, Tanzi says that scientists are just beginning to scratch the surface of the culprits who can spark the spiral into Alzheimer's disease.
This is one of the reasons why Tanzi's laboratory scientists map the brain's microbiome – the population of microorganisms, useful or pathological, that exists in the brain – using samples autopsied brain positive for Alzheimer's disease. . The Brain Microbiome project researchers are researching the most common germs in the brain to try to determine which ultimately lead to Alzheimer's disease. With the information, they hope to develop therapeutic products to prevent and treat the disease that is expected to destroy the brains of nearly 14 million Americans by 2050.
Tanzi, Robert Moir and their Harvard's team of researchers have found more evidence this month of the belief that microbes are indeed at the heart of Alzheimer's disease. The team reported in the journal Neuron findings that suggest that herpes viruses can trigger the cascade of events that leads to Alzheimer's disease.
In separate experiments, the researchers studied the response of neurons to the presence of herpes. simplex 1 (HSV-1), the virus that causes herpes labialis and herpes virus 6 (HHV-6), the virus that causes skin disease of childhood roseola . (Most people catch these viruses early in life and, typically, they stay dormant, but as they age, they almost always migrate to the brain.)
In these experiments, scientists genetically raised certain mice to gain neurons. this could create the human version of a protein called beta-amyloid. Normally produced in the brain, beta-amyloid would be responsible for the plaques that would ultimately lead to Alzheimer's disease.
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Tanzi says, since 2010, that his research has shown that:
- Amyloid beta protein is an antimicrobial. peptide produced and used by the brain to protect itself against germs.
- But for unknown reasons, beta amyloid protein is overproduced in people with Alzheimer's and encourages the brain to engage in processes that ultimately lead to the disease. kill or trap (squeeze) microbes to protect the brain. But doing so, in patients with Alzheimer's, the process creates an accumulation of amyloid plaques.
- These plaques trigger the production of entanglements of another brain protein called tau in the brain, which will then cause chronic inflammation and eventually the question became: "If amyloid has the ability to be antimicrobial, so what are the microbes in the brain that trigger the plaques? ", said Tanzi
. Tanzi said his team showed that herpes viruses could "quickly" induce amyloid plaque production in mice (within 24 to 48 hours); that the plaques trap the virus to protect the brain cells from viral infection; and that mice raised with the ability to create beta-amyloid were better able to fight brain infection than mice without it. "So, amyloid is trying to do a good job of protecting the brain, but too many problems are causing it," Tanzi said.
Tanzi concluded that it is "the seeding of amyloid" that causes plaque formation. "And herpes viruses and other microbes can quickly spawn beta-amyloid," he said.
It is not the only one to point fingers at viruses as precursors of dementia. He said researchers at Mount Sinai Medical Center were the first to find an overabundance of herpes virus in autopsied brains of people with Alzheimer's disease. This team of researchers from the Icahn School of Medicine at Mount Sinai also recently published an article in Neuron supporting the role of viruses in Alzheimer's disease. His labs and those of Mount Sinai have corroborated this topic for a while, he says.
Tanzi warns however that the fact that a person has one of the herpes viruses does not mean that she will suffer from Alzheimer's disease. "We are not saying that herpes viruses cause Alzheimer's disease, we suggest that they are a risk factor that causes the formation of plaques that can later become Alzheimer's," she said. he said. "Just because you're positive for these viruses does not mean you have Alzheimer's disease. It simply means that we know that it activates the process that causes Alzheimer's disease more often. These viruses are the tip of the iceberg. Fungus, viruses, bacteria – there are dozens of microbes. A Taiwanese newspaper recently showed a broad epidemiological segment of people on antiviral drugs, specifically anti-herpes, which were protected against Alzheimer's disease. The question will be which microbes beyond herpes play the biggest role in triggering amyloid in the brain. "
Meanwhile, the brain microbiome mapping continues." In the end, once we have a list of the most common microbes – that it's about bacteria, viruses or yeasts – we'll think of antimicrobial drugs, "said Dr. Tanzi." Once we know what are the most common microbes in the Alzheimer's brain that trigger amyloid production, we can start developing treatments. "
He said that these treatments would vary greatly, including preventative antimicrobial drugs – vaccines that can prevent the germs from reaching the brain in the first place. the plates should be used early, but also the drugs against inflammation, as well as drugs that can attack the microbial infection that can trigger the plaques, "he said.
And that do not stop p There are other things that trigger plaques, including genetics, "said Tanzi. "We need to know what else.The infection acts like a seed.Other seeds could be an air pollution that is just the right size to get into the nose and cross the blood-brain barrier and mimic microbes. "
Dr. Rudolph E. Tanzi, Vice President of Neurology, Director of the Genetics and Aging Research Unit at Massachusetts General Hospital, and Professor of Neurology Joseph P. and Rose F. Kennedy at Harvard Medical School . Dr. Rudolph E. Tanzi)
But for now, Tanzi's focus is on microbes. And some would say that his opinion is worth taking into consideration. Tanzi has co-discovered three of the first genes of Alzheimer's disease and has identified several others in the Alzheimer's Genome Project, which he directs. He also discovered the Wilson's disease gene and participated in the discovery of several other neurological disease genes. Using a neural culture system derived from three-dimensional human stem cells that he created, Tanzi is also developing therapeutic products for Alzheimer's disease including gamma secretase modulators and metal chaperones to reduce the beta-cell burden. amyloid and entanglement in the brain
. Among the 100 most influential people in the world, Tanzi has published nearly 500 research papers and received the highest awards in his field, including the Metropolitan Life Foundation Award and the Potamkin Award and the Smithsonian American Ingenuity Award. He co-wrote the business books "Decoding Darkness", "Super Brain" and "Super Genes".
Tanzi says that he believes that doctors will manage Alzheimer's disease – as they do today – from here 2025 otherwise
And he is in good company. Scientists across the United States go a long way to developing treatments for dementia. In an article published in Elsevier's Alzheimer's & Dementia: Translational Research & Clinical Interventions, Jeffrey Cummings, of Lou Ruvo Center of the Cleveland Clinic for Brain Health reports that there was in January 2018, 112 agents in the Alzheimer's disease pipeline treatment. Of these, Cummings reports that "63% are disease-modifying therapies, 22% are symptomatic cognitive enhancers, and 12% are symptomatic agents addressing neuropsychiatric and behavioral changes." (Cummings is based on the US). registered clinical activity in clinicaltrials.gov Federal law requires that all clinical trials conducted in the United States be registered on the site.) And the drug development pipeline against Alzheimer's disease is bigger this year than ever before. 39, in 2017.
Although there was a setback, Tanzi's own drug developed with his colleague Steve Wagner of the University of California at San Diego (UCSD) and the National Neuropsapeutics Network of National Institutes of Health (NIH) is expected to be in clinical trials by 2019. Called "Gamma Modulator (GSM)," Tanzi believes that it will at least be part of the prescription to stop the pathol Alzheimer's disease leads to symptoms. He said that scientists over the last year have developed a "stronger, safer" version of the drug.
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Finally, it will be microbes – bacteria, viruses and fungi – that will be at the origin of everything, Dr. Rudolph" Rudy "Emile Tanzi, geneticist, said:" The two most Great threats to healthy aging relate to infection, "said Tanzi, a specialist in Alzheimer's Disease and Brain, at Massachusetts General Hospital (MGH) and at Harvard. Medical School. "Think about it, when we increased the life span from 35 to 50, that's by covering the sewers. We are now looking for viruses in all the major life-threatening diseases of our time – Alzheimer's disease, cancer, Parkinson's disease – and guess what … The infection is in the process of multiply in all cases.
Mount who could prove his theory, T Anzi says that scientists are just starting to scratch the surface of the culprits who can trigger the spiral in Alzheimer's disease.
This is one of the reasons why Tanzi's laboratory scientists are mapping the brain's microbiome – the population of microorganisms. useful and some pathological, which exists inside the brain-using autopsied brain samples that have been tested positive for the pathology of Alzheimer's disease. The Brain Microbiome project researchers are researching the most common germs in the brain to try to determine which ultimately lead to Alzheimer's disease. With the information, they hope to develop therapeutic products to prevent and treat the disease that is expected to destroy the brains of nearly 14 million Americans by 2050.
Tanzi, Robert Moir and their Harvard's team of researchers have found more evidence this month of the belief that microbes are indeed at the heart of Alzheimer's disease. The team reported in the journal Neuron findings that suggest that herpesviruses can trigger the cascade of events leading to Alzheimer's disease.
In separate experiments, the researchers studied the response of neurons to the presence of herpes. simplex 1 (HSV-1), the virus that causes herpes labialis and herpes virus 6 (HHV-6), the virus that causes skin disease of childhood roseola . (Most people catch these viruses early in life and, typically, they stay dormant, but as they age, they almost always migrate to the brain.)
In these experiments, scientists genetically raised certain mice to gain neurons. this could create the human version of a protein called beta-amyloid. Normally produced in the brain, beta-amyloid is considered responsible for the plaques that ultimately lead to Alzheimer's disease.
Tanzi says, since 2010, his research has shown that:
- Amyloid beta protein is an antimicrobial peptide produced and used But for unknown reasons, beta amyloid protein is overproduced in people suffering from the disease. Alzheimer's and encourages the brain to engage in processes that ultimately lead to the disease.
- Neurons use beta-amyloid to kill or trap (agglutinate) microbes to protect the brain. But doing so, in patients with Alzheimer's, the process creates an accumulation of amyloid plaques.
- These plaques trigger the production of entanglements of another brain protein called tau in the brain, which will then cause chronic inflammation and eventually the question became: "If amyloid has the ability to be antimicrobial, so what are the microbes in the brain that trigger the plaques? ", said Tanzi
. Tanzi said his team showed that herpes viruses could "quickly" induce amyloid plaque production in mice (within 24 to 48 hours); that the plaques trap the virus to protect the brain cells from viral infection; and that mice raised with the ability to create beta-amyloid were better able to fight brain infection than mice without it. "So, amyloid is trying to do a good job of protecting the brain, but too many problems are causing it," Tanzi said.
Tanzi concluded that it is "the seeding of amyloid" that causes plaque formation. "And herpes viruses and other microbes can quickly spawn beta-amyloid," he said.
It is not the only one to point fingers at viruses as precursors of dementia. He said researchers at Mount Sinai Medical Center were the first to find an overabundance of herpes virus in autopsied brains of people with Alzheimer's disease. This team of researchers from the Icahn School of Medicine at Mount Sinai also recently published an article in Neuron supporting the role of viruses in Alzheimer's disease. His labs and those of Mount Sinai have corroborated this topic for a while, he says.
Tanzi warns however that the fact that a person has one of the herpes viruses does not mean that she will suffer from Alzheimer's disease. "We are not saying that herpes viruses cause Alzheimer's disease, we suggest that they are a risk factor that causes the formation of plaques that can later become Alzheimer's," she said. he said. "Just because you're positive for these viruses does not mean you have Alzheimer's disease. It simply means that we know that it activates the process that causes Alzheimer's disease more often. These viruses are the tip of the iceberg. Fungus, viruses, bacteria – there are dozens of microbes. A Taiwanese newspaper recently showed a broad epidemiological segment of people on antiviral drugs, specifically anti-herpes, which were protected against Alzheimer's disease. The question will be which microbes beyond herpes play the biggest role in triggering amyloid in the brain. "
Meanwhile, the brain microbiome mapping continues." In the end, once we have a list of the most common microbes – that it's about bacteria, viruses or yeasts – we'll think of antimicrobial drugs, "said Dr. Tanzi." Once we know what are the most common microbes in the Alzheimer's brain that trigger amyloid production, we can start developing treatments. "
He said that these treatments would vary greatly, including preventative antimicrobial drugs – vaccines that can prevent the germs from reaching the brain in the first place. the plates should be used early, but also the drugs against inflammation, as well as drugs that can attack the microbial infection that can trigger the plaques, "he said.
And that do not stop p There are other things that trigger plaques, including genetics, "said Tanzi. "We need to know what else.The infection acts like a seed.The other seeds could be air pollution which is just the right size to penetrate the nose and cross the barrier hemato-encephalic and imitate microbes. "
Dr. Rudolph E. Tanzi, Vice President of Neurology, Director of the Genetics and Aging Research Unit at Massachusetts General Hospital, and Professor of Neurology Joseph P. and Rose F. Kennedy at Harvard Medical School . Dr. Rudolph E. Tanzi)
But for now, Tanzi's focus is on microbes. And some would say that his opinion is worth taking into consideration. Tanzi has co-discovered three of the first genes of Alzheimer's disease and has identified several others in the Alzheimer's Genome Project, which he directs. He also discovered the Wilson's disease gene and participated in the discovery of several other neurological disease genes. Using a neural culture system derived from three-dimensional human stem cells that he created, Tanzi is also developing therapeutic products for Alzheimer's disease including gamma secretase modulators and metal chaperones to reduce the beta-cell burden. amyloid and entanglement in the brain
. Among the 100 most influential people in the world, Tanzi has published nearly 500 research papers and received the highest awards in his field, including the Metropolitan Life Foundation Award and the Potamkin Award and the Smithsonian American Ingenuity Award. He co-wrote the business books "Decoding Darkness", "Super Brain" and "Super Genes".
Tanzi says that he believes that doctors will manage Alzheimer's disease – as they do today – from here 2025 otherwise
And he is in good company. Scientists across the United States go a long way to developing treatments for dementia. In an article published in Elsevier's Alzheimer's & Dementia: Translational Research & Clinical Interventions, Jeffrey Cummings, of Lou Ruvo Center of the Cleveland Clinic for Brain Health reports that there was in January 2018, 112 agents in the Alzheimer's disease pipeline treatment. Of these, Cummings reports that "63% are disease-modifying therapies, 22% are symptomatic cognitive enhancers, and 12% are symptomatic agents addressing neuropsychiatric and behavioral changes." (Cummings is based on the US). registered clinical activity in clinicaltrials.gov Federal law requires that all clinical trials conducted in the United States be registered on the site.) And the drug development pipeline against Alzheimer's disease is bigger this year than ever before. 39, in 2017.
Although there was a setback, Tanzi's own drug developed with his colleague Steve Wagner of the University of California at San Diego (UCSD) and the National Neuropsapeutics Network of National Institutes of Health (NIH) is expected to be in clinical trials by 2019. Called "Gamma Modulator (GSM)," Tanzi believes that it will at least be part of the prescription to stop the pathol Alzheimer's disease leads to symptoms. He said that scientists over the past year have developed a "stronger, safer" version of the drug.
