7
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Targeting small Abeta oligomers: the solution to an Alzheimer's disease conundrum?

      Trends in Neurosciences
      Alzheimer Disease, drug therapy, metabolism, Amyloid beta-Peptides, drug effects, pharmacology, Amyloid beta-Protein Precursor, Animals, Antibodies, therapeutic use, Hippocampus, Long-Term Potentiation, physiology, Mice, Mice, Transgenic, Peptide Fragments, Plaque, Amyloid, Signal Transduction, Synaptophysin, Vaccines

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Amyloid beta (Abeta) is a small self-aggregating peptide produced at low levels by normal brain metabolism. In Alzheimer's disease (AD), self-aggregation of Abeta becomes rampant, manifested most strikingly as the amyloid fibrils of senile plaques. Because fibrils can kill neurons in culture, it has been argued that fibrils initiate the neurodegenerative cascades of AD. An emerging and different view, however, is that fibrils are not the only toxic form of Abeta, and perhaps not the neurotoxin that is most relevant to AD: small oligomers and protofibrils also have potent neurological activity. Immuno-neutralization of soluble Abeta-derived toxins might be the key to optimizing AD vaccines that are now on the horizon.

          Related collections

          Author and article information

          Comments

          Comment on this article