Skip to main content
padlock icon - secure page this page is secure

Modulation of Amyloid β Peptide1-42 Cytotoxicity and Aggregation in Vitro by Glucose and Chondroitin Sulfate

Buy Article:

$68.00 + tax (Refund Policy)

One mechanism leading to neurodegeneration during Alzheimer's Disease (AD) is amyloid β peptide (Aβ)- induced neurotoxicity. Among the factors proposed to potentiate Aβ toxicity is its covalent modification through carbohydrate- derived advanced glycation endproducts (AGEs). Other experimental evidence, though, indicates that certain polymeric carbohydrates like the glycosaminoglycan (GAG) chains found in proteoglycan molecules attenuate the neurotoxic effect of Aβ in primary neuronal cultures. Pretreatment of the 42-residue Aβ fragment (Aβ1-42) with the ubiquitous brain carbohydrates, glucose, fructose, and the GAG chondroitin sulfate B (CSB) inhibits Aβ1-42-induced apoptosis and reduces the peptide neurotoxicity on neuroblastoma cells, a cytoprotective effect that is partially reverted by AGE inhibitors such as pyridoxamine and L-carnosine. Thioflavin T fluorescence measurements indicate that at concentrations close to physiological, only CSB promotes the formation of Aβ amyloid fibril structure. Atomic force microscopy imaging and Western blot analysis suggest that glucose favours the formation of globular oligomeric structures derived from aggregated species. Our data suggest that at short times carbohydrates reduce Aβ1-42 toxicity through different mechanisms both dependent and independent of AGE formation.





No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Keywords: Alzheimer's disease; advanced glycation endproducts; amyloid fibrils; amyloid β peptide; apoptosis; carbohydrates; glycosaminoglycans

Document Type: Research Article

Publication date: August 1, 2010

More about this publication?
  • Current Alzheimer Research publishes peer-reviewed frontier review and research articles on all areas of Alzheimer's disease. This multidisciplinary journal will help in understanding the neurobiology, genetics, pathogenesis, and treatment strategies of Alzheimer's disease. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, molecular, and animal models. The journal also covers original articles on recent research in fast emerging areas of molecular diagnostics, brain imaging, drug development and discovery, and clinical aspects of Alzheimer's disease. Manuscripts are encouraged that relate to the synergistic mechanism of Alzheimer's disease with other dementia and neurodegenerative disorders. Book reviews, meeting reports and letters-to-the-editor are also published. The journal is essential reading for researchers, educators and physicians with interest in age-related dementia and Alzheimer's disease. Current Alzheimer Research provides a comprehensive 'bird's-eye view' of the current state of Alzheimer's research for neuroscientists, clinicians, health science planners, granting, caregivers and families of this devastating disease.
  • Editorial Board
  • Information for Authors
  • Subscribe to this Title
  • Ingenta Connect is not responsible for the content or availability of external websites
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more