Pathological mechanism

Data

Name Ginkgolides protect against amyloid-beta1-42-mediated synapse damage in vitro.

Description

Hypothesis Synapse Loss Show Other

Extracelular pathological element beta Amyloid Show Other

Intracelular pathological element

Pathological action Induces Show Other

Process Synapse Loss Show Other

Process action

Transmitter(s)

Receptor(s)

Channel(s)

Pharmacological Agent Gingkolides Show Other

Pharmacological Action Protects Show Other

Brain region Hippocampus CA1 Show Other Visual cortex Show Other

Neuron

Cell model Cultured cortical neurons Show Other

Cellular compartment

PubMed ID 18179689

Citation

AlzWeb

Notes The addition of Abeta1-42 to cortical or hippocampal neurons reduced the amounts of cell associated synaptophysin, a pre-synaptic membrane protein that is essential for neurotransmission, indicating synapse damage. The effects of Abeta1-42 on synapses were apparent at concentrations approximately 100 fold less than that required to kill neurons; the synaptophysin content of neuronal cultures was reduced by 50% by 50 nM Abeta1-42. Pre-treatment of cortical or hippocampal neuronal cultures with ginkgolides A or B, but not with myrecitin or quercetin, protected against Abeta1-42-induced loss of synaptophysin. Bate, C., Tayebi, M., & Williams, A. (2008). Ginkgolides protect against amyloid-beta1-42-mediated synapse damage in vitro. Molecular Neurodegeneration, 3, 1.

Pathology Alzheimer Show Other

Stage Early Show Other

Question Exclude - dietary factors, no electrophysiology

Claim