Pathological mechanism

Data

Name Abeta inhibits LTP both in soluble and fibrillar conformational states

Description Abeta1-40 peptide in soluble and fibrillar forms (beta pleated sheets) that are morphologically distinct can both attenuate hippocampal long-term potentiation (LTP) in the CA1 in vivo. The fibrillar form may also influence transmitter release.

Hypothesis LTP hypothesis Show Other

Extracelular pathological element beta Amyloid Show Other

Intracelular pathological element

Pathological action Inhibits Show Other

Process LTP Show Other

Process action

Transmitter(s)

Receptor(s)

Channel(s)

Pharmacological Agent

Pharmacological Action

Brain region Hippocampus CA1 Show Other

Neuron Hippocampus CA1 pyramidal GLU cell Show Other

Cell model

Cellular compartment General or unspecified Show Other

PubMed ID 18237717

Citation

AlzWeb

Notes Abeta1-40 peptide in soluble and fibrillar forms (beta pleated sheets) that are morphologically distinct can both attenuate hippocampal long-term potentiation (LTP) in the CA1 in vivo. The fibrillar form may also influence transmitter release.Schmid, A. W., Freir, D. B., & Herron, C. E. (2008). Inhibition of LTP in vivo by beta-amyloid peptide in different conformational states. Brain Res, 1197, 135-142.

Pathology Alzheimer Show Other

Stage Early Show Other

Question

Claim