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• Alzheimer's disease: a re-examination of the amyloid hypothesis.
• Citation:
  Neve R, Robakis N
  

  Alzheimer's disease: a re-examination of the amyloid hypothesis.

  Trends in neurosciences. 1998 Jan;21(1):15-9
  [PubMed] [Alzforum]
• Supporting:
  • It has been postulated that abnormal processing of APP to Aβ, or reduced clearance of Aβ from brain, resulting in the parenchymal aggregation of Aβ to form amyloid deposits is an early and crucial event in the pathogenesis of the disease

    SHOW Details   Supporting(3) 

    Experimental Approach: Mechanism - molecular and cell,  
    Pathogenic Narrative Tags: Pathogenic event
    Supporting Evidence
    

    • Selkoe D
      Cell biology of the amyloid beta-protein precursor and the mechanism of Alzheimer's disease.
      Annual review of cell biology. 1994;10:373-403
    • Hardy J, Higgins G
      Alzheimer's disease: the amyloid cascade hypothesis.
      Science (New York, N.Y.). 1992 Apr 10;256(5054):184-5
    • Neve R, Robakis N
      Alzheimer's disease: a re-examination of the amyloid hypothesis.
      Trends in neurosciences. 1998 Jan;21(1):15-9
  • Abnormal processing of APP to Aβ, or reduced clearance of Aβ from brain, results in the parenchymal aggregation of Aβ to form amyloid deposits which is an early and crucial event in the pathogenesis of the disease.

    SHOW Details   Supporting(3)   Consistent(1)   Alternative to: (1)

    Experimental Approach: Mechanism - biochemistry and structural biology
    Pathogenic Narrative Tags:
    Supporting Evidence
    

    • Neve R, Robakis N
      Alzheimer's disease: a re-examination of the amyloid hypothesis.
      Trends in neurosciences. 1998 Jan;21(1):15-9
    • Selkoe D
      Cell biology of the amyloid beta-protein precursor and the mechanism of Alzheimer's disease.
      Annual review of cell biology. 1994;10:373-403
    • Hardy J, Higgins G
      Alzheimer's disease: the amyloid cascade hypothesis.
      Science (New York, N.Y.). 1992 Apr 10;256(5054):184-5

    Consistent statements
    

    • Protein aggregation is a central event in the initiation of cell death in neurodegenerative diseases. Keck S  Nitsch R  Grune T  Ullrich O 

    Alternative statements
    

    • In extensive studies, no clear correlation between deposited forms of Aβ (such as plaques) and memory impairment in AD patients has been demonstrated. Dodart J  Bales K  Gannon K  Greene S  DeMattos R  Mathis C  DeLong C  Wu S  Wu X  Holtzman D  Paul S 
• Discussed by:
  No alternative hypothesis with as much experimental support as the amyloid hypothesis can explain the cause and pathogenesis of AD, despite discussion on the deficiencies of the amyloid hypothesis.
  SHOW Details   Discussing: (3)  Consistent(2) 
  Experimental Approach:
  Pathogenic Narrative Tags:
  Discussing Evidence
  
  • Davies P
    A very incomplete comprehensive theory of Alzheimer's disease.
    Annals of the New York Academy of Sciences. 2000;924:8-16
  • Neve R, Robakis N
    Alzheimer's disease: a re-examination of the amyloid hypothesis.
    Trends in neurosciences. 1998 Jan;21(1):15-9
  • Roses A
    Apolipoprotein E affects the rate of Alzheimer disease expression: beta-amyloid burden is a secondary consequence dependent on APOE genotype and duration of disease.
    Journal of neuropathology and experimental neurology. 1994 Sep;53(5):429-37
  Consistent statements
  
  • The prevailing amyloid hypothesis posits that accumulation of Aβ peptides, particularly the more hydrophobic and aggregation-prone Aβ42, triggers a pathogenic cascade, leading to neurodegeneration in AD. Shen J  Kelleher R 
  • Because EOAD and late-onset AD (LOAD) phenocopy each other clinically and histologically, the amyloid hypothesis—although based on molecular defects isolated in EOAD—was plausibly proposed to underlie all forms of the disease. Small S  Duff K 
• Created On: Wed, Apr 23 06:44:08 EDT 2008
• Last Modified On: Wed Apr 23 06:44:08 EDT 2008