The Journal of Membrane Biology

, Volume 202, Issue 1, pp 1–10 | Cite as

Amyloid Peptide Channels

  • B.L. KaganEmail author
  • R. Azimov
  • R. Azimova
Topical Review


At least 16 distinct clinical syndromes including Alzheimer’s disease (AD), Parkinson’s disease (PD), rheumatoid arthritis, type II diabetes mellitus (DM), and spongiform encephelopathies (prion diseases), are characterized by the deposition of amorphous, Congo red-staining deposits known as amyloid. These “misfolded” proteins adopt β-sheet structures and aggregate spontaneously into similar extended fibrils despite their widely divergent primary sequences. Many, if not all, of these peptides are capable of forming ion-permeable channels in vitro and possibly in vivo. Common channel properties include irreversible, spontaneous insertion into membranes, relatively large, heterogeneous single-channel conductances, inhibition of channel formation by Congo red, and blockade of inserted channels by Zn2+. Physiologic effects of amyloid, including Ca2+ dysregulation, membrane depolarization, mitochondrial dysfunction, inhibition of long-term potentiation (LTP), and cytotoxicity, suggest that channel formation in plasma and intracellular membranes may play a key role in the pathophysiology of the amyloidoses.


Alzheimer’s Amyloid deposits Prion Pores Lipid bilayers Aβ channels 



Part of this work was supported by grants from the Alzheimer’s Association, NINCDS, and NIMH


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© Springer-Verlag 2004

Authors and Affiliations

  1. 1.Department of Psychiatry, Neuropsychiatric Institute, David Geffen School of MedicineUCLALos AngelesUSA

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