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• Early-onset behavioral and synaptic deficits in a mouse model of Alzheimer's disease.
• Citation:
  Jacobsen J, Wu C, Redwine J, Comery T, Arias R, Bowlby M, Martone R, Morrison J, Pangalos M, Reinhart P, Bloom F
  

  Early-onset behavioral and synaptic deficits in a mouse model of Alzheimer's disease.

  Proceedings of the National Academy of Sciences of the United States of America. 2006 Mar 28;103(13):5161-6
  [PubMed] [Alzforum]
• Supporting:
  • Recent studies have demonstrated that soluble Aβ species correlate with onset of memory and synaptic plasticity impairments before detectable amyloid plaques.

    SHOW Details   Supporting(2)   Consistent(4) 

    Experimental Approach: Pathophysiology,   Mechanism - molecular and cell,   Neuropsychology/Behavior,   Mechanism - biochemistry and structural biology
    Pathogenic Narrative Tags: Pathogenic event
    Supporting Evidence
    

    • Jacobsen J, Wu C, Redwine J, Comery T, Arias R, Bowlby M, Martone R, Morrison J, Pangalos M, Reinhart P, Bloom F
      Early-onset behavioral and synaptic deficits in a mouse model of Alzheimer's disease.
      Proceedings of the National Academy of Sciences of the United States of America. 2006 Mar 28;103(13):5161-6
    • Lesné S, Koh M, Kotilinek L, Kayed R, Glabe C, Yang A, Gallagher M, Ashe K
      A specific amyloid-beta protein assembly in the brain impairs memory.
      Nature. 2006 Mar 16;440(7082):352-7

    Consistent statements
    

    • Amyloid is the consequence, not the cause, of AD.
      Smith M, Perry G, Castellani R, Lee H Wed, Feb 10 2010 17:25:40 EST SHOW Details 
      Rather than amyloid being responsible for causing disease, we suspect that Alzheimer Disease is responsible for causing amyloid. In fact, amyloid may even be a protective response. As such, removing amyloid would be predicted to either have no effect or a detrimental effect on AD progression.
      

      • Joseph et al., 2001
      • Smith et al., 2002
      • Lee et al., 2004
      • Smith et al., 2002
      • Perry et al., 2000
      • Atwood et al., 2002
      • Lee et al., 2006
    • Three global cognitive tests (Blessed IMC, MMSE and Total DRS) demonstrated by far the closest correlation to the density of mid-frontal (MF) presynaptic boutons, and to inferior parietal (IP) synapse density to a lesser extent. Terry R  Masliah E  Salmon D  Butters N  DeTeresa R  Hill R  Hansen L  Katzman R 
    • Changes in the density of the presynaptic marker synaptophysin are better correlated with disease progression than Aβ plaque load or cell death. Dziewczapolski G  Glogowski C  Masliah E  Heinemann S 
    • In transgenic mouse and rat models with Aβ deposition, synaptic changes occur before plaque accumulation, evidence that gives strength to the idea that the soluble nonfibrillary species of Aβ plays a crucial role in AD pathogenesis. Dziewczapolski G  Glogowski C  Masliah E  Heinemann S 
• Created On: Thu, Apr 24 17:06:33 EDT 2008
• Last Modified On: Thu Apr 24 17:06:33 EDT 2008