Vascular dysfunction-associated with Alzheimer's disease

Cristiana Carelli Alinovi, Francesco Misiti, Simone Dinarelli, Marco Girasole

Risultato della ricerca: Contributo in rivistaArticolo in rivista

7 Citazioni (Scopus)

Abstract

Our attention is focused on the study of a new model based on the red blood cell (RBC) and on its interaction with amyloid beta peptide 1-42 (Aβ). RBC are highly deformable to assist blood flow in the microcirculation. For this reasons RBC abnormalities could contribute to Alzheimer's disease (AD) by obstructing oxygen delivery to brain, causing hypoxia. In our work, considering that RBC membrane contains, among blood elements, higher acetylcholinesterase (AChE) levels, we can assume that in blood occurs a mechanism similar to the one which occurs at the neuronal level leading to an increase of Aβ toxicity mediated by its binding with AChE, located on the RBC external face. Furthermore, since mechanical properties of RBC membrane are regulated by a number of molecular components of signalling and/or regulatory pathways, of these, particular interest has been addressed toward Nitric Oxide (NO) metabolism, due to its dependence to AChE.
Lingua originaleEnglish
pagine (da-a)679-687-687
RivistaClinical Hemorheology and Microcirculation
Volume64
DOI
Stato di pubblicazionePubblicato - 2016

Keywords

  • Alzheimer disease
  • Amyloid beta peptide
  • NO metabolites
  • acetylcholinesterase
  • nitric oxide synthase
  • red blood cell

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