Heparan sulfate and chondroitin sulfate glycosaminoglycan attenuate β-amyloid(25–35) induced neurodegeneration in cultured hippocampal neurons

摘要: Abstract β-Amyloid peptide has been reported to be toxic neurons in vitro and vivo. The fragment of the β1–42 believed responsible for this toxicity consists amino acids 25 35. protein, heparan sulfate (HS) glycosaminoglycan (GAG), proteoglycan (PG) are all localized throughout senile plauqes found Alzheimer's disease. Chondroitin (CS) dermatan have also at periphery plaques. We that both HS CS prevented neurite fragmentation normally induced by β25–35. themselves did not a significant influence on cell viability, indicating their protective actions were due general trophic effect. In contrast, cultures treated with show significantly reduced compared alone despite specific binding interactions. These data indicate one function GAGs brain may protect from select insults injury, additionally suggest interacts differently different β-amyloid fragments. further fragments induce distinct mechanisms vitro.