Reduction in plaque formation

Christian Czech, Helmut Jacobsen, Celine Adessi, Bruno P. Imbimbo, Francesca Speroni, Dario Cattaneo, Harry LeVine, Corinne E. Augelli-Szafran

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


Alzheimer’s Disease (AD) is a progressive and neurodegenerative disorder of the brain characterized by loss of neurons and synapses, particularly in regions related to memory and cognition. The main neuropathological features of AD are accumulation of abnormal intracellular and extracellular proteinaceous deposits in the brain of the patients (Alois Alzheimer in 1907)-within neuronal cells, as accumulation of abnormally phosphorylated tau protein into paired helical ?laments, known as neuro?brillary tangles (NFTs) (Terry, 1994) and outside cellular structures as proteinaceous aggregates in form of amyloid plaques and as amyloid in the wall of cerebral blood vessels (Masters et al., 1985; Selkoe, 1991). The sequence of pathological events leading to the observed deposits and ?nally to neurodegeneration is believed to start with the abnormal processing of the amyloid precursors protein (APP), leading to the generation of Ab (Kang et al., 1987). The hypothesis states that the Ab protein triggers through formation of toxic aggregates the subsequent formation of NFTs, loss of synapses, and ?nally loss of neuronal function. This sequence of events is now described as the amyloid cascade (Figure 4.1).

Original languageEnglish
Title of host publicationProtein Misfolding in Neurodegenerative Diseases
Subtitle of host publicationMechanisms and Therapeutic Strategies
Number of pages120
ISBN (Electronic)9781420007145
StatePublished - Jan 1 2007

Bibliographical note

Publisher Copyright:
© 2008 by Taylor & Francis Group, LLC.

ASJC Scopus subject areas

  • General Chemistry
  • General Medicine
  • General Biochemistry, Genetics and Molecular Biology
  • General Neuroscience


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