MSGID: 1:317/3 64781f0d   
   PID: hpt/lnx 1.9.0-cur 2019-01-08   
   TID: hpt/lnx 1.9.0-cur 2019-01-08   
    Tracking early signs of Alzheimer's pathology in a mouse model    
    Behavioral interventions may alter trajectory    
      
     Date:   
         May 31, 2023   
     Source:   
         Elsevier   
     Summary:   
         About two-thirds of the risk for Alzheimer's disease (AD) is   
         thought to arise from genetic influences, but about a third   
         could be influenced by environment and lifestyle, opening the   
         door for behavioral interventions that could delay or prevent   
         pathophysiological changes that occur with AD. Now a new study in a   
         mouse model of AD examines the effects of environmental enrichment   
         on AD symptom progression and pathology.   
      
      
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   FULL STORY   
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   About two-thirds of the risk for Alzheimer's disease (AD) is thought to   
   arise from genetic influences, but about a third could be influenced by   
   environment and lifestyle, opening the door for behavioral interventions   
   that could delay or prevent pathophysiological changes that occur with   
   AD. Now a new study in a mouse model of AD examines the effects of   
   environmental enrichment on AD symptom progression and pathology. The   
   study appears in Biological Psychiatry, published by Elsevier.   
      
   Gerd Kempermann, PhD, from the German Center for Neurodegenerative   
   Diseases in Dresden, Germany, and senior author of the study, emphasized   
   the importance of studying the early stages of disease, when interventions   
   might be most effective.   
      
   Dr. Kempermann commented, "AD does not start when the symptoms become   
   obvious.   
      
   There is a decades-long silent period, during which the pathology   
   progresses undetected. Clinicians and researchers have become increasingly   
   interested in what happens during this phase."  To study this early   
   pathology, Dr. Kempermann and colleagues used a mouse model of AD that   
   replicates this silent period. The model contains several mutations   
   associated with human AD in the gene encoding amyloid precursor protein   
   (App).   
      
   These AppNL-F mice develop toxic amyloid-beta plaques by age 6 months   
   and cognitive impairment by 18 months.   
      
   Dr. Kempermann said, "However, we discovered that there are already subtle   
   but important behavioral changes long before the first plaques appear,   
   and the cognitive deficits become detectable."  The mice were housed   
   in an enriched environment, which consisted of 60 interconnected cages,   
   from age 6 weeks to 23 weeks and were then moved to standard cages after   
   4 months. Living in the enriched environment improved several measures   
   of metabolism, which are known risk factors for AD.   
      
   Dr. Kempermann explained, "The [AD model] mice in our study showed   
   a reduction in individual behaviors. They became more similar and   
   more rigid. As this individualization is to a large degree driven by   
   individual behavior and depends on brain plasticity, we can conclude   
   that the affected mice had behavioral deficits very early in the   
   course of the disease. They did not respond normally to the offerings   
   of their environment. This finding is important, because it will help   
   us to understand how we can best tailor preventive measures during   
   the pre-clinical phase. It also underscores that prevention has to   
   start early."  The researchers also examined markers of neurogenesis in   
   the mice.   
      
   Paradoxically, the AppNL-F mice had higher rates of neurogenesis than   
   control mice, which is interpreted as a failing attempt at compensation   
   and as paradoxically counterproductive. This overshooting compensation   
   was normalized by exposure to enrichment.   
      
   John Krystal, MD, Editor of Biological Psychiatry, said of the work,   
   "This novel study suggests that environmental enrichment may reduce   
   the early accumulation of amyloid plaques in a mouse model of AD. This   
   insight may suggest a strategy for delaying the development of symptoms   
   associated with this disorder."   
       * RELATED_TOPICS   
             o Health_&_Medicine   
                   # Alzheimer's_Research # Healthy_Aging #   
                   Parkinson's_Research # Chronic_Illness   
             o Mind_&_Brain   
                   # Alzheimer's # Dementia # Behavior # Huntington's_Disease   
       * RELATED_TERMS   
             o Alzheimer's_disease o Mouse o Personalized_medicine o   
             Delayed_puberty o Dementia_with_Lewy_bodies o Animal_cognition   
             o Homosexuality o House_mouse   
      
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   Story Source: Materials provided by Elsevier. Note: Content may be edited   
   for style and length.   
      
      
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   Journal Reference:   
      1. Fanny Ehret, Meike S. Pelz, Anna N. Senko, Karla E.G. Soto,   
      Hang Liu,   
         Gerd Kempermann. Pre-symptomatic reduction of individuality in   
         the App NL-F knock-in model of Alzheimer's disease. Biological   
         Psychiatry, 2023; DOI: 10.1016/j.biopsych.2023.04.009   
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   Link to news story:   
   https://www.sciencedaily.com/releases/2023/05/230531150058.htm   
      
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