Protein intake is known to be vital for maintaining brain function in older individuals. Now, using a mouse model of Alzheimer’s disease, researchers have shown that the intake of a specific set of amino acids can inhibit the death of brain cells, protect the connections between them, and reduce inflammation, preserving brain function. Their research suggests that this amino acid combination called Amino LP7 can hinder the development of dementia, including Alzheimer’s disease.
One explanation for this could be the degree of efficiency of each organism’s response to the damage sustained by its cells during its life, which eventually causes them to age. In relation to this, researchers at the Universitat Oberta de Catalunya (UOC) and the University of Leicester (United Kingdom) have developed a new method to remove old cells from tissues, thus slowing down the aging process.
No one knows why some people age worse than others and develop diseases-such as Alzheimer’s, fibrosis, type 2 diabetes or some types of cancer-associated with this aging process. One explanation for this could be the degree of efficiency of each organism’s response to the damage sustained by its cells during its life, which eventually causes them to age. In relation to this, researchers at the Universitat Oberta de Catalunya (UOC) and the University of Leicester (United Kingdom) have developed a new method to remove old cells from tissues, thus slowing down the aging process.
Specifically, they have designed an antibody that acts as a smart bomb able to recognize specific proteins on the surface of these aged or senescent cells. It then attaches itself to them and releases a drug that removes them without affecting the rest, thus minimizing any potential side effects.
The results of this work, which have been published in Scientific Reports, open the door to the development of effective treatments to delay the progress of age-related diseases and even the aging process itself in the longer term, with the aim of increasing the longevity and, above all, the quality of life of people at this stage of their lives.
Roche’s gantenerumab is an anti-amyloid beta antibody developed for subcutaneous administration in Alzheimer’s disease patients.
Roche’s gantenerumab, an anti-amyloid beta antibody developed for subcutaneous administration, has been granted Breakthrough Therapy Designation by the US Food and Drug Administration (FDA) for the treatment of people living with Alzheimer’s disease (AD).
BCIs stands out as one of the most promising assistive technologies.
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All your movements start out in your brain.
When you decided that you wanted to read this article, you planned on moving your finger (or your cursor) toward a certain spot on your screen. Without noticing it, you thought about pressing or clicking on that spot. After quickly processing that thought, your brain told your muscles to respond to it accordingly, and here you are.
But the muscles of people with paralysis do not react to these brain signals. The brain might be unable to send the signals, the spinal cord might fail to deliver them to the nerves, or the nerves might not respond to them. This can be due to congenital or acquired damage in any of these parts of the nervous system.
Only a matter of time til we can have nanobots clearing this out.
In a major breakthrough, researchers at Massachusetts General Hospital (MGH) have discovered how amyloid beta — the neurotoxin believed to be at the root of Alzheimer’s disease (AD) — forms in axons and related structures that connect neurons in the brain, where it causes the most damage. Their findings, published in Cell Reports, could serve as a guidepost for developing new therapies to prevent the onset of this devastating neurological disease.
Among his many contributions to research on AD, Rudolph Tanzi, PhD, vice chair of Neurology and co-director of the McCance Center for Brain Health at MGH, led a team in 1986 that discovered the first Alzheimer’s disease gene, known as APP, which provides instructions for making amyloid protein precursor (APP). When this protein is cut (or cleaved) by enzymes — first, beta secretase, followed by gamma secretase — the byproduct is amyloid beta (sometimes shortened to Abeta). Large deposits of amyloid beta are believed to cause neurological destruction that results in AD. Amyloid beta formed in the brain’s axons and nerve endings causes the worst damage in AD by impairing communication between nerve cells (or neurons) in the brain. Researchers around the world have worked intensely to find ways to block the formation of amyloid beta by preventing cleavage by beta secretase and gamma secretase. However, these approaches have been hampered by safety issues.
Despite years of research, a major mystery has remained. “We knew that Abeta is made in the axons of the brain’s nerve cells, but we didn’t know how,” says Tanzi. He and his colleagues probed the question by studying the brains of mice, as well as with a research tool known as Alzheimer’s in a dish, a three-dimensional cell culture model of the disease created in 2014 by Tanzi and a colleague, Doo Yeon Kim, PhD. Earlier, in 2,013 several other MGH researchers, including neurobiologist Dora Kovacs, PhD (who is married to Tanzi), and Raja Bhattacharyya, PhD, a member of Tanzi’s lab, showed that a form of APP that has undergone a process called palmitoylation (palAPP) gives rise to amyloid beta. That study indicated that, within the neuron, palAPP is transported in a fatty vesicle (or sac) known as a lipid raft. But there are many forms of lipid rafts.
Integrated And Cross-Disciplinary Research Focused on Diagnosing, Treating And Curing Cancers — Dr. Antonio Giordano MD, PhD, President & Founder, Sbarro Health Research Organization.
Dr. Antonio Giordano, MD, Ph.D., (https://www.drantoniogiordano.com/) is President and Founder of the Sbarro Health Research Organization (https://www.shro.org/), which conducts research to diagnose, treat and cure cancer, but also has diversified into research beyond oncology, into the areas of cardiovascular disease, diabetes and other chronic illnesses.
Dr. Giordano is also a Professor of Molecular Biology at Temple University in Philadelphia, a ‘Chiara fama’ Professor in the Department of Pathology & Oncology at the University of Siena, Italy, and Director of the Sbarro Institute for Cancer Research and Molecular Medicine, and the Center for Biotechnology, at Temple’s College of Science & Technology.
In his research throughout the years, Dr. Giordano has identified numerous tumor suppressor genes, including Rb2/p130, which has been found to be active in lung, endometrial, brain, breast, liver and ovarian cancers, as well as interesting synergistic effects of gamma radiation in combination with this gene, accelerating the death of tumor cells.
Dr. Giordano went on to discover Cyclin A, Cdk9 (which is known to play critical roles in HIV transcriptions, inception of tumors, and cell differentiation), and Cdk10. Dr. Giordano also developed patented technologies for diagnosing cancer.
For most of the time since the first description of multiple sclerosis (MS) in 1,868 the causes of this disabling disease have remained uncertain. Genes have been identified as important, which is why having other family members with MS is associated with a greater risk of developing the disease.
A recent study my colleagues and I conducted found that several types of infection during the teenage years are associated with MS after age 20. Our study didn’t investigate whether people who are more likely to have genetic risks for MS were also more likely to have worse infections.
This might explain why people with MS also have more infections that need hospital treatment.
Photosynthesizing algae injected into the blood vessels of tadpoles supply oxygen to their brains.
Leading a double life in water and on land, frogs have many breathing techniques – through the gills, lungs, and skin – over the course of their lifetime. Now German scientists have developed another method that allows tadpoles to “breathe” by introducing algae into their bloodstream to supply oxygen. The method developed, presented October 13 in the journal iScience, provided enough oxygen to effectively rescue neurons in the brains of oxygen-deprived tadpoles.
“The algae actually produced so much oxygen that they could bring the nerve cells back to life, if you will,” says senior author Hans Straka of Ludwig-Maximilians-University Munich. “For many people, it sounds like science fiction, but after all, it’s just the right combination of biological schemes and biological principles.”