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   Herpes linked to Alzheimer's disease: 'Cold sores' connected to cognitive   
   decline   
      
   Date:   
   April 4, 2011   
   Source:   
   Brown University   
   Summary:   
   New research using a new technique to observe herpes simplex virus type 1   
   infections inside cells, finds that re-activation and growth of HSV1   
   infections contribute to cognitive decline associated with Alzheimer's disease.   
      
      
   Laboratories at the University of New Mexico (UNM), Brown University, and   
   House Ear Institute (HEI) have developed a new technique to observe herpes   
   simplex virus type 1 (HSV1) infections growing inside cells. HSV1, the cause   
   of the common cold sore,    
   persists in a latent form inside nerve cells. Re-activation and growth of HSV1   
   infections contribute to cognitive decline associated with Alzheimer's disease.   
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   Details are published in the March 31 issue of PLoS ONE.   
   "Herpes infects mucous membranes, such as the lip or eye, and generates viral   
   particles," submits study Principal Investigator Elaine Bearer, M.D., Ph.D.,   
   Harvey Family Professor and Vice Chair for Research, Department of Pathology,   
   UNM School of    
   Medicine. "These viral particles burst out of the cells of the mucous membrane   
   and enter sensory nerve cells where they travel inside the nerve toward the   
   brain. We now can see this cellular transportation system and watch how the   
   newly formed virus    
   engages cellular APP on its journey out of the cell."   
   Tagging herpes virus inside cells with green fluorescent protein, scientists   
   used live confocal imaging to watch HSV1 particles emerge from infected cells.   
   Newly produced viral particles exit the cell nucleus and then bud into   
   cellular membranes    
   containing amyloid precursor protein (APP). Electron microscopy at HEI   
   detailed the ultrastructural relationship between HSV1 particles and APP.   
   This dance between viral particles and cellular APP results in changes in   
   cellular architecture and the distribution of APP, the major component of   
   senile plaques found in the brains of Alzheimer's disease patients. Results   
   from this study indicate that    
   most intracellular HSV1 particles undergo frequent, dynamic interplay with   
   APP, which facilitates viral transport while interfering with normal APP   
   transport and distribution. This dynamic interaction reveals a mechanism by   
   which HSV1 infection leads to    
   Alzheimer's disease.   
   In developed countries such as the U.S., approximately 20 percent of children   
   are infected with HSV1 prior to the age of five. By the second and third   
   decades of life, as much as 60 percent of the population is infected, and   
   late-in-life infection rate    
   reaches 85 percent.   
   Symptoms of primary HSV1 infection include painful blisters of the mouth, lips   
   or eyes. After infection, HSV1 persists in nerve cells by becoming latent.   
   Upon re-awakening, new viral particles are made in the neuron and then travel   
   back out its pathways    
   to re-infect the mucous membrane. Many infected people experience sporadic   
   episodes of viral outbreaks as the well-known recurrent cold sore.   
   "Clinicians have seen a link between HSV1 infection and Alzheimer's disease in   
   patients, so we wanted to investigate what might be going on in the body that   
   would account for this," adds Dr. Shi-Bin Cheng, post-doctoral associate,   
   Department of Pathology    
   and Laboratory Medicine, Alpert Medical School, Brown University. "What we   
   were able to see in the lab strongly suggests a causal link between HSV1 and   
   Alzheimer's Disease."   
   "It's no longer a matter of determining whether HSV1 is involved in cognitive   
   decline, but rather how significant this involvement is," Bearer asserts.   
   "We'll need to investigate anti-viral drugs used for acute herpes treatment to   
   determine their ability    
   to slow or prevent cognitive decline."   
   Researchers recommend people treat a cold sore as quickly as possible to   
   minimize the amount of time the virus is actively traveling through a person's   
   nervous system. The faster a cold sore is treated, the faster the HSV1 returns   
   to a dormant stage.   
   Additional Authors include: Paulette Ferland, senior research assistant, UNM;   
   Paul Webster, House Ear Institute, Los Angeles, CA; participation of Kathleen   
   Kilpatrck, UNM; and many undergraduate students at Brown who contributed to   
   this project are    
   acknowledged.   
   Story Source:   
   The above story is based on materials provided by Brown University. Note:   
   Materials may be edited for content and length.   
   Journal Reference:   
   Shi-Bin Cheng, Paulette Ferland, Paul Webster, Elaine L. Bearer. Herpes   
   Simplex Virus Dances with Amyloid Precursor Protein while Exiting the Cell.   
   PLoS ONE, 2011; 6 (3): e17966 DOI: 10.1371/journal.pone.0017966   
   Cite This Page:   
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   Brown University. "Herpes linked to Alzheimer's disease: 'Cold sores'   
   connected to cognitive decline." ScienceDaily. ScienceDaily, 4 April 2011.   
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