{"id":110423,"date":"2024-07-11T22:00:49","date_gmt":"2024-07-11T17:00:49","guid":{"rendered":"https:\/\/pni.net.pk\/en\/?p=110423"},"modified":"2024-07-11T17:09:28","modified_gmt":"2024-07-11T12:09:28","slug":"study-finds-possible-new-target-for-early-treatment-of-alzheimers-disease","status":"publish","type":"post","link":"https:\/\/pni.net.pk\/en\/latest-health-news\/study-finds-possible-new-target-for-early-treatment-of-alzheimers-disease\/","title":{"rendered":"Study finds possible new target for early treatment of Alzheimer&#8217;s disease"},"content":{"rendered":"<pre class=\"aLF-aPX-K0-aPE\">ISLAMABAD, July 11 (Online): With an aging population worldwide, neurodegenerative diseases, such as dementia, are an increasing problem.\r\nAlthough there are treatments for neurodegenerative diseases, these generally alleviate symptoms, rather than changing the course of the disease.\r\nNow, research has found that a protein that regulates cell repair could be a promising new target for treating several of these conditions, including the most common, Alzheimer\u2019s disease.\r\nNeurodegenerative diseasesTrusted Source occur when nerve cells in the brain and peripheral nervous system lose function and eventually die. They include Alzheimer\u2019s disease, Parkinson\u2019s diseaseTrusted Source, and amyotrophic lateral sclerosisTrusted Source (ALS \u2014 also known as motor neuron disease), among others.\r\n\r\nIn the United States, an estimated 6.9 million people aged 65 and over are living with Alzheimer\u2019s disease, and around a million have Parkinson\u2019s. ALS is less common; the CDC estimates that around 31,000 peopleTrusted Source in the U.S. have the condition.\r\n\r\nCurrent treatments can alleviate symptoms and some slow the progression of the diseases, but no cures are yet available. New monoclonal antibody treatments for Alzheimer\u2019s have shown some potential for modifying the course of the disease, but many experts are concerned about side effects.\r\n\r\nIn the search for new therapies, research from Penn State University has identified a group of proteins that could be a target for new treatments for Alzheimer\u2019s and other neurodegenerative disorders.\r\n\r\nThe researchers, who have a patent related to this work, found that reducing the function of heparan-sulfate-modified proteoglycans (HSPGs) helped reverse cell damage from neurodegenerative diseases.\r\n\r\nTheir study is published iniScienceTrusted Source.\r\n\r\n\u201cThis is interesting research which shows how cells might be protected from the effects of genetic mutations that cause Alzheimer\u2019s disease. However, as it has only been shown in fruit flies and human cells from outside of the brain, it\u2019s hard to say just how relevant the findings are at the moment. We\u2019re excited to see the next stage of this research, to see if similar effects can be seen in human brain cells.\u201d\r\n\r\n\u2014 Katherine Gray, Alzheimer\u2019s Society\u2019s head of research\r\n\r\n\r\nProteins influence cell repair\r\nHSPGs, which are found on the surface of cells and in the extracellular matrix, regulate cell repair and enhance cell growth-signaling systems. The heparan sulfate (sugar) chainsTrusted Source attach to proteins so they can influence processes including cell growth, interaction between the cell and its environment, and autophagy \u2014 a process that clears out protein aggregates (a feature of Alzheimer\u2019s disease) and damaged parts of cells.\r\n\r\nResearch leader Scott Selleck, professor of biochemistry and molecular biology at the Penn State Eberly College of Science, said in a press release:\r\n\r\n\u201cIn the early stages of several neurodegenerative diseases, autophagy is compromised, which means cells have a reduced repair capacity.\u201d\r\n\r\nReducing proteins\u2019 effects reversed neurodegenerative changes\r\n\u201cIn this study, we determined that heparan sulfate-modified proteins suppress autophagy-dependent cell repair. What\u2019s more, we show that by compromising the structure and function of the sugar modifications of these proteins, the levels of autophagy increase so cells can take care of damage.\r\n\r\n\u2014 Scott Selleck, research leader\r\n\r\nStudies have noted heparan sulfate abnormalities in Alzheimer\u2019s disease, but their specific role in the development of the disorder has not yet been uncovered.\r\n\r\nBy carrying out analyses on human cell lines and mouse brain cells that express aspects of Alzheimer\u2019s, researchers in this study first showed that HSPGs regulate cell processes that are affected in several neurodegenerative diseases.\r\n\r\nThey then reduced the function of the HSPGs in these cells and found that two changes that happen early in the course of neurodegenerative diseases were reversed. The function of the mitochondria \u2014 which provide energy for the cell \u2014 was improved, and that lipid (fat) buildup in the cells was reduced.\r\n\r\n\r\nAnimal model findings\r\nTo verify their findings, the researchers used an animal model of Alzheimer\u2019s. They used fruit flies that had been modified to have deficits in presenilin protein, which mimics the effect of a mutation in the presenilin gene, PSEN1Trusted Source, the most common cause of familial (early-onset) Alzheimer\u2019s.\r\n\r\nSelleck explained that a rare genetic changeTrusted Source in another protein, APOE, can delay the effect of the PSEN1 mutation, sometimes for decades. He suggested that targeting these two substances and the enzymes that make heparan sulfate could help prevent neurodegeneration in people.\r\n\r\nIn the fruit flies, the researchers reduced the functioning of HSPGs, which suppressed the death of nerve cells and corrected other cell defects.\r\n\r\nThey suggest that disrupting the structure of heparan sulfate modifications blocks or reverses early cellular problems in these models of Alzheimer\u2019s.\r\n\r\nPotential treatment for early stage neurodegeneration\r\nSelleck highlighted the potential of the team\u2019s findings:\r\n\r\n\u201cThere is a critical need to focus on cellular changes that occur at the earliest times in disease progression and develop treatments that block or reverse them,\u201d he said in a press release.\r\n\r\n\u201cWe demonstrate that reduced autophagy, mitochondrial defects and lipid build-up \u2014 all common changes in neurodegenerative disease \u2014 can be blocked by altering one class of proteins, those with heparan sulfate modifications. We think these molecules are promising targets for drug development,\u201d he added.\r\n\r\nCourtney Kloske, Ph.D., Alzheimer\u2019s Association director of scientific engagement, welcomed the findings but emphasized that further research was needed:\r\n\r\n\u201cThis interesting but very preliminary study is based on research in a fruit fly model of Alzheimer\u2019s. While animal models of the disease are somewhat similar to how Alzheimer\u2019s progresses in humans, they do not replicate the disease in humans exactly.\u201d\r\n\r\n\u201cModels are important in helping us understand the basic biology of the disease, but we need human studies in representative populations for ideas to be fully validated. Therefore, more research is needed to understand the possible role of heparan sulfate-modified proteins in Alzheimer\u2019s as studied in this manuscript\u201d she told Medical News Today.<\/pre>\n","protected":false},"excerpt":{"rendered":"<p>ISLAMABAD, July 11 (Online): With an aging population worldwide, neurodegenerative diseases, such as dementia, are an increasing problem. Although there are treatments for neurodegenerative diseases, these generally alleviate symptoms, rather than changing the course of the disease. Now, research has found that a protein that [&#8230;]<\/p>\n<p>\n","protected":false},"author":16,"featured_media":110424,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[9821],"tags":[],"class_list":["post-110423","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-latest-health-news"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.1.1 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Study finds possible new target for early treatment of Alzheimer&#039;s disease<\/title>\n<meta name=\"description\" content=\"Study finds possible new target for early treatment of Alzheimer&#039;s disease\" \/>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" 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