[ad_1]
<div _ngcontent-c14 = "" innerhtml = "
Researchers at the University of Texas (UT) announced Tuesday that they have developed a vaccine that could arm the body against Alzheimer's plaques and tangles even before they start to stop the disease. brain. They hope to start testing the vaccines in humans soon.
Getty
For the first time, their new vaccine targets both amyloid-containing plates and tau, both considered essential for the definitive identification of Alzheimer's disease, in a mouse with the disease.
The shot uses DNA from Alzheimer's proteins to teach the immune system to fight these compounds and prevent them from accumulating in the brain. Researchers say their new vaccine against Alzheimer's disease, called DNA Aβ42– could possibly halve the number of cases of dementia.
The new vaccine – unlike a previous attempt that had caused swelling of the brain when DNA had been injected into the test mouse muscles – was administered by superficial injection into the skin. The injected skin cells then form a chain of three beta-amyloid molecules, and the body reacts by producing antibodies that drive away amyloid and tau formation.
"The importance of these results is that Aβ DNA42 Trimer immunotherapy targets two major pathologies of AD: amyloid plaques and neurofibrillary tangles – in a vaccine without inducing an inflammatory response of T cells, which presents a danger of autoimmune inflammation ", writes the lead author, Roger N. Rosenberg, founding director of the National Institutes of Health (NIH) funded by the Alzheimer's Disease Center of the Department of Neurology and Neurotherapeutics of southwestern UT. Co-authors include Min Fu and Doris Lambracht-Washington, also from the UT Southwestern Medical Center in Dallas, Texas.The researchers published their findings in the journal, Alzheimer's and research therapy, a BMC Series newspaper publication.
As researchers do not know when amyloid and tau begin to form, Rosenberg said doctors would determine when to administer the vaccine by performing amyloid brain scans and PET tau.
Although Rosenberg's research has nothing to do with Rudolph Tanzi's, the Harvard scientist who co-discovered the three family genes of Alzheimer's disease and who runs the Cure Alzheimer's Fund Alzheimer's Genome Project, their premises are similar. Keep the amyloid down. Avoid Alzheimer's disease.
Tanzi's Massachusetts General Hospital (MGH) laboratory maps the brain's microbiome – the population of microorganisms, some useful and some pathological, existing in the brain – using autopsied brain samples positive for Alzheimer's disease. Brain Microbiome researchers are researching the most common germs found in the brain to determine which ones eventually lead to Alzheimer's disease. With this information, they hope to develop treatments to prevent and treat the disease.
This apart from the three-dimensional system of neuronal culture derived from human stem cells (or organoid of the simulated human brain), "Alzheimer's-in-aa-Dish", which Tanzi and his colleague, Dr. Doo Yeon Kim, created with the genes d & # 39; Alzheimer's. This system essentially reproduces the processes of plaque and entanglement of Alzheimer's disease. Using this system, Tanzi has developed a drug for Alzheimer's disease, including gamma secretase modulators and metal chaperones, to reduce beta amyloid and entanglement in the brain.
Although the research is incredibly complex, scientists have used stem cells to create human nerve cells. They then put them in a gel to simulate the human brain and thus created a real Alzheimer's pathology in a petri dish, thus allowing them to have a first real view of the events that usually occur at the Over the decades, the formation of amyloid plaques leading to entanglements and inflammation – in the brain, he says.
Alzheimer's-in-a-Dish has solved the argument that goes back several decades, whether amyloid plaques or tangles are responsible for Alzheimer's disease, said Tanzi. "There is no more debate," he said. "All the data say that if you keep the amyloid weak, you stop Alzheimer's."
Similar to Rosenberg's quest to stop Alzheimer's disease before it begins, Tanzi believes that the need for early intervention and treatment of dementia is cancer and heart disease. "Unlike heart disease and cancer, we do not diagnose and treat Alzheimer's before the symptoms begin, and then we treat the cause, the amyloid plaques. We had to stop amyloid plaques 10 to 20 years before the person had symptoms. "
Tanzi said that we can now determine the possibility that a person contracted later in Alzheimer's disease uses brain imaging and biomarkers while she is still asymptomatic, as do doctors with cholesterol tests for heart disease. He added that the time had not yet come when blood tests would also be available for the treatment of Alzheimer's disease.
In the same way that Americans are now taking a drug to prevent cholesterol buildup, Tanzi hopes he will take one to lower the level of his amyloid proteins in the brain. "One day, once we have an effective and safe anti-amyloid drug, everyone will see their amyloid checked at age 50, say, as they do with a colonoscopy. If you have a higher than normal amount, you can take a medicine to prevent the onset of Alzheimer's dementia symptoms. In 2025, I think we will be there. If all goes well, a mobile phone may be available within five years. "
Or maybe they'll just have Rosenberg's vaccine.
"We report, for the first time in an AD mouse model, that Aβ active DNA42 Vaccination in skin targets two pathologies: plaques containing amyloid and tau protein, "the UT researchers wrote in their study. "DNA vaccination, which consists of administering not the antigen (peptide or protein) but the DNA coding for this peptide, is another route of vaccination. The genes encoded by the DNA are expressed in the skin and the peptides are captured by the dendritic cells moving to the regional lymph nodes and presenting the antigen to the B and T cells.
UT researchers have already shown that complete Aβ DNA42 Immunization with trimer is non-inflammatory and induces a measurable immune response.42 Trimer immunization has been shown to be effective in eliminating brain amyloid in immunized double transgenic mice, "the researchers wrote." They have now discovered that immunotherapy by the 39; Aβ DNA42 trimer leads to the reduction of amyloid peptides and amyloid plaques as well as "… for the first time42 Immunization with trimer also results in a significant reduction of mouse brain tau protein. "
Neurodegenerative disease, Alzheimer's disease is the most common form of dementia in the aging population. Rosenberg and others have been arguing for years that immunotherapy targeting beta amyloid (Aβ) accumulation in amyloid may be a therapeutic option and help prevent the progression of the disease. A number of vaccination approaches were unsuccessful, including one that was discontinued after the researchers noted the development of autoimmune encephalitis in 6% of their patients.
Getty
Today, Alzheimer's disease is the 6th main cause of death in the United States. It paralyzes the brains of those who are affected as the beta-amyloid proteins of the brain stick together and form entanglements of tau proteins that inhibit neuronal connections. There is no cure and so far, only symptomatic treatment options are available.
The pathological features of amyloid plaques and neurofibrillary tangles are considered essential for definitive identification of Alzheimer's disease. And the origin and development of the disease have been strongly associated with the accumulation and clustering of beta-amyloid in the brain. Nearly 30 years ago, the hypothesis of an amyloid cascade was formulated, according to which amyloid deposition is the initial event leading to Alzheimer's disease.
Injected into the skin, Rosenberg's vaccine proved that it resulted in the cells' production of skin from a chain of three molecules of beta-amyloid. Anticipating plaques and Alzheimer's tangles before they are formed, the immune system is then activated to produce antibodies that fight beta-amyloid and tau proteins.
Research at UT has tested four groups of mice. About 40% of beta-amyloid plaques were reduced in vaccinated mice and up to 50% of their tau interferences decreased. The researchers said they observed no adverse immune response with the vaccine. According to the researchers, the results show that "with the vaccine, the body is armed and ready to attack the plaques and Alzheimer's tangles before they start to stop the brain."
US scientists are working to develop treatments for dementia. In an Elsevier article titled Alzheimer's and Dementia: Translational Research and Clinical Interventions, Jeffrey Cummings of the Lou Ruvo Center for Brain Health Research at the Cleveland Clinic reported that in January 2018 there were 112 agents in the treatment of Alzheimer's disease. Cummings reports that "63% are disease-modifying therapies, 22% symptomatic cognitive enhancers, and 12% symptomatic agents treating neuropsychiatric and behavioral changes." (The Cummings Journal is based on clinical trial activity recorded in cliniquetrials.gov., A comprehensive database of the US Government. 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 larger this year than in 2017.
">
Researchers at the University of Texas (UT) announced Tuesday that they have developed a vaccine that could arm the body against Alzheimer's plaques and tangles even before they start to stop the disease. brain. They hope to start testing the vaccines in humans soon.
For the first time, their new vaccine targets both amyloid-containing plates and tau, both considered essential for the definitive identification of Alzheimer's disease, in a mouse with the disease.
The shot uses DNA from Alzheimer's proteins to teach the immune system to fight off these compounds and prevent them from accumulating in the brain. Researchers say their new vaccine against Alzheimer's disease, called DNA Aβ42– could possibly halve the number of cases of dementia.
The new vaccine – unlike a previous attempt that had caused swelling of the brain when DNA had been injected into the test mouse muscles – was administered by superficial injection into the skin. The injected skin cells then form a chain of three beta-amyloid molecules, and the body reacts by producing antibodies that drive away amyloid and tau formation.
"The importance of these results is that Aβ DNA42 Trimer immunotherapy targets two major pathologies of AD: amyloid plaques and neurofibrillary tangles – in a vaccine without inducing an inflammatory response of T cells, which presents a danger of autoimmune inflammation ", writes the lead author, Roger N. Rosenberg, founding director of the National Institutes of Health (NIH) funded by the Alzheimer's Disease Center of the Department of Neurology and Neurotherapeutics of southwestern UT. Co-authors include Min Fu and Doris Lambracht-Washington, also from the UT Southwestern Medical Center in Dallas, Texas.The researchers published their findings in the journal, Alzheimer's and research therapy, a BMC Series newspaper publication.
As researchers do not know when amyloid and tau begin to form, Rosenberg said doctors would determine when to administer the vaccine by performing amyloid brain scans and PET tau.
Although Rosenberg's research has nothing to do with Rudolph Tanzi's, the Harvard scientist who co-discovered the three family genes of Alzheimer's disease and who runs the Cure Alzheimer's Fund Alzheimer's Genome Project, their premises are similar. Keep the amyloid down. Avoid Alzheimer's disease.
Tanzi's Massachusetts General Hospital (MGH) laboratory maps the brain's microbiome – the population of microorganisms, some useful and some pathological, existing in the brain – using autopsied brain samples positive for Alzheimer's disease. Brain Microbiome researchers are researching the most common germs found in the brain to determine which ones eventually lead to Alzheimer's disease. With this information, they hope to develop treatments to prevent and treat the disease.
This apart from the three-dimensional system of neuronal culture derived from human stem cells (or organoid of the simulated human brain), "Alzheimer's-in-aa-Dish", which Tanzi and his colleague, Dr. Doo Yeon Kim, created with the genes d & # 39; Alzheimer's. This system essentially reproduces the processes of plaque and entanglement of Alzheimer's disease. Using this system, Tanzi has developed a drug for Alzheimer's disease, including gamma secretase modulators and metal chaperones, to reduce beta amyloid and entanglement in the brain.
Although the research is incredibly complex, scientists have used stem cells to create human nerve cells. They then put them in a gel to simulate the human brain and thus created a real Alzheimer's pathology in a petri dish, thus allowing them to have a first real view of the events that usually occur at the Over the decades, the formation of amyloid plaques leading to entanglements and inflammation – in the brain, he says.
Alzheimer's-in-a-Dish has solved the argument that goes back several decades, whether amyloid plaques or tangles are responsible for Alzheimer's disease, said Tanzi. "There is no more debate," he said. "All the data say that if you keep the amyloid weak, you stop Alzheimer's."
Similar to Rosenberg's quest to stop Alzheimer's disease before it begins, Tanzi believes that the need for early intervention and treatment of dementia is cancer and heart disease. "Unlike heart disease and cancer, we do not diagnose and treat Alzheimer's before the symptoms begin, and then we treat the cause, the amyloid plaques. We had to stop amyloid plaques 10 to 20 years before the person had symptoms. "
Tanzi said that we can now determine the possibility that a person contracted later in Alzheimer's disease uses brain imaging and biomarkers while she is still asymptomatic, as do doctors with cholesterol tests for heart disease. He added that the time had not yet come when blood tests would also be available for the treatment of Alzheimer's disease.
In the same way that Americans are now taking a drug to prevent cholesterol buildup, Tanzi hopes he will take one to lower the level of his amyloid proteins in the brain. "One day, once we have an effective and safe anti-amyloid drug, everyone will see their amyloid checked at age 50, say, as they do with a colonoscopy. If you have a higher than normal amount, you can take a medicine to prevent the onset of Alzheimer's dementia symptoms. In 2025, I think we will be there. If all goes well, a mobile phone may be available within five years. "
Or maybe they'll just have Rosenberg's vaccine.
"We report, for the first time in an AD mouse model, that Aβ active DNA42 Vaccination in skin targets two pathologies: plaques containing amyloid and tau protein, "the UT researchers wrote in their study. "DNA vaccination, which consists of administering not the antigen (peptide or protein) but the DNA coding for this peptide, is another route of vaccination. The genes encoded by the DNA are expressed in the skin and the peptides are captured by the dendritic cells moving to the regional lymph nodes and presenting the antigen to the B and T cells.
UT researchers have already shown that complete Aβ DNA42 Immunization with trimer is non-inflammatory and induces a measurable immune response.42 Trimer immunization has been shown to be effective in eliminating brain amyloid in immunized double transgenic mice, "the researchers wrote." They have now discovered that immunotherapy by the 39; Aβ DNA42 trimer leads to the reduction of amyloid peptides and amyloid plaques as well as "… for the first time42 Immunization with trimer also results in a significant reduction of mouse brain tau protein. "
Neurodegenerative disease, Alzheimer's disease is the most common form of dementia in the aging population. Rosenberg and others have been arguing for years that immunotherapy targeting beta amyloid (Aβ) accumulation in amyloid may be a therapeutic option and help prevent the progression of the disease. A number of vaccination approaches were unsuccessful, including one that was discontinued after the researchers noted the development of autoimmune encephalitis in 6% of their patients.
Today, Alzheimer's disease is the 6th main cause of death in the United States. It paralyzes the brains of those who are affected as the beta-amyloid proteins of the brain stick together and form entanglements of tau proteins that inhibit neuronal connections. There is no cure and so far, only symptomatic treatment options are available.
The pathological features of amyloid plaques and neurofibrillary tangles are considered essential for definitive identification of Alzheimer's disease. And the origin and development of the disease have been strongly associated with the accumulation and clustering of beta-amyloid in the brain. Nearly 30 years ago, the hypothesis of an amyloid cascade was formulated, according to which amyloid deposition is the initial event leading to Alzheimer's disease.
Injected into the skin, Rosenberg's vaccine proved that it resulted in the cells' production of skin from a chain of three molecules of beta-amyloid. Anticipating plaques and Alzheimer's tangles before they are formed, the immune system is then activated to produce antibodies that fight beta-amyloid and tau proteins.
Research at UT has tested four groups of mice. About 40% of beta-amyloid plaques were reduced in vaccinated mice and up to 50% of their tau interferences decreased. The researchers said they observed no adverse immune response with the vaccine. According to the researchers, the results show that "with the vaccine, the body is armed and ready to attack the plaques and Alzheimer's tangles before they start to stop the brain."
US scientists are working to develop treatments for dementia. In an Elsevier article titled Alzheimer's and Dementia: Translational Research and Clinical Interventions, Jeffrey Cummings of the Lou Ruvo Center for Brain Health Research at the Cleveland Clinic reported that in January 2018 there were 112 agents in the treatment of Alzheimer's disease. Cummings reports that "63% are disease-modifying therapies, 22% symptomatic cognitive enhancers, and 12% symptomatic agents treating neuropsychiatric and behavioral changes." , a comprehensive database of the US government. Federal law requires all clinical trials conducted in the United States to be registered on the site.) And the Alzheimer's Drug Development pipeline is larger this year than in 2017.
