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   Message 7,774 of 8,931   
   ScienceDaily to All   
   Fresh understanding of aging in the brai   
   08 Mar 23 21:30:44   
   
   MSGID: 1:317/3 640960f6   
   PID: hpt/lnx 1.9.0-cur 2019-01-08   
   TID: hpt/lnx 1.9.0-cur 2019-01-08   
    Fresh understanding of aging in the brain offers hope for treating   
   neurological diseases    
      
     Date:   
         March 8, 2023   
     Source:   
         Trinity College Dublin   
     Summary:   
         Scientists have shed new light on aging processes in the brain. By   
         linking the increased presence of specialized immune cells to   
         conditions such as Alzheimer's disease and traumatic brain injury   
         for the first time, they have unearthed a possible new target for   
         therapies aimed at treating age-related neurological diseases.   
      
      
         Facebook Twitter Pinterest LinkedIN Email   
   FULL STORY   
   ==========================================================================   
   Scientists from the Trinity Biomedical Sciences Institute (TBSI)   
   have shed new light on ageing processes in the brain. By linking the   
   increased presence of specialised immune cells to conditions such as   
   Alzheimer's disease and traumatic brain injury for the first time, they   
   have unearthed a possible new target for therapies aimed at treating   
   age-related neurological diseases.   
      
      
   ==========================================================================   
   The research, which benefited from a collaboration with experts at the   
   University of Maryland School of Medicine and focused on microglia in   
   the brain and spinal cord, is published today in leading international   
   journal, Science Advances.   
      
   Microglia are a unique type of immune cell whose job it is to support   
   nerve cells, defend against invading microbes, clear debris and remove   
   dying nerve cells by engulfing and eating them. Emerging research   
   indicates that microglia can have different functional responses   
   depending on molecular and biochemical changes occurring within these   
   specialised cells.   
      
   In fact, various subtypes of microglia can be distinguished based on a   
   property called autofluorescence. This is the tendency of cells to emit   
   light of one colour after they have absorbed light of another, and it   
   occurs because specific substances inside the cells absorb light. The   
   substances stored in specialised cellular compartments include fat   
   molecules, cholesterol crystals, metals and other misfolded proteins.   
      
   David Loane, Assistant Professor of Neuroscience in Trinity's School   
   of Biochemistry and Immunology in TBSI is the lead author of the   
   research. He said: "As the brain ages, these materials build up inside   
   autofluorescent microglia, which increase their autofluorescence as   
   a result. Unfortunately, this accumulation of cellular debris also   
   makes it harder for the microglia to perform their essential garbage   
   collection tasks in the brain and to prevent neurological injury and   
   neurodegenerative disease.   
      
   "In this study we found -- in aged animals -- that these microglia   
   adopt a unique, dysfunctional state, which has a number of problematic   
   impacts. For example, there is an increase in cellular stress and damage,   
   an accumulation of fats and iron, alterations to metabolic processes and   
   an increase in production of molecules that over-egg the immune response."   
   In addition, the scientists demonstrated that autofluorescent microglia   
   and associated inflammation were more pronounced under pathological   
   conditions, such as in genetic risk factor models of Alzheimer's disease,   
   and - - promisingly -- were reversed by drug-assisted microglial   
   replacement in aged animals.   
      
   Prof Loane added: "Furthermore, environmental exposure to acute traumatic   
   brain injury in animals accelerated the age of onset and tissue-wide   
   distribution autofluorescent microglia by increasing oxidative stress   
   damage in the brain of injured animals.   
      
   "As a result, increasing evidence now suggests that the accumulation   
   of autofluorescent microglia contributes to diseases of ageing and   
   neurodegeneration. If these sub-populations of microglia are highly   
   inflammatory and damaging to the brain, then targeting them could be a   
   new strategy for treating aging-related diseases."   
       * RELATED_TOPICS   
             o Health_&_Medicine   
                   # Brain_Tumor # Nervous_System # Immune_System #   
                   Healthy_Aging   
             o Mind_&_Brain   
                   # Brain_Injury # Neuroscience # Disorders_and_Syndromes   
                   # Dementia   
       * RELATED_TERMS   
             o Brain_damage o Traumatic_brain_injury o   
             Excitotoxicity_and_cell_damage o Alzheimer's_disease o   
             Urinary_incontinence o Cerebral_contusion o Embryonic_stem_cell   
             o Stem_cell   
      
   ==========================================================================   
   Story Source: Materials provided by Trinity_College_Dublin. Note:   
   Content may be edited for style and length.   
      
      
   ==========================================================================   
   Journal Reference:   
      1. Rodney M. Ritzel, Yun Li, Yun Jiao, Zhuofan Lei, Sarah J. Doran,   
      Junyun   
         He, Rami A. Shahror, Rebecca J. Henry, Romeesa Khan, Chunfeng   
         Tan, Shaolin Liu, Bogdan A. Stoica, Alan I. Faden, Gregory Szeto,   
         David J.   
      
         Loane, Junfang Wu. Brain injury accelerates the onset of a   
         reversible age-related microglial phenotype associated with   
         inflammatory neurodegeneration. Science Advances, 2023; 9 (10)   
         DOI: 10.1126/ sciadv.add1101   
   ==========================================================================   
      
   Link to news story:   
   https://www.sciencedaily.com/releases/2023/03/230308171550.htm   
      
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