Pathological mechanism

Data

Name Nicotine decreases intracellular copper concentration; attenuates Abeta toxicity

Description

Hypothesis Nicotinic Receptor Hypothesis Show Other

Extracelular pathological element Nicotine Show Other

Intracelular pathological element Copper Show Other

Pathological action Reduces Show Other

Process

Process action

Transmitter(s)

Receptor(s)

Channel(s)

Pharmacological Agent

Pharmacological Action

Brain region Hippocampus CA1 Show Other

Neuron

Cell model Brain slice preparations Show Other

Cellular compartment

PubMed ID 16627626

Citation

AlzWeb

Notes Zhang, J., Liu, Q., Chen, Q., Liu, N. Q., Li, F. L., Lu, Z. B., et al. (2006). Nicotine attenuates beta-amyloid-induced neurotoxicity by regulating metal homeostasis. The FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology, 20(8), 1212-1214. Nicotine treatment decreases the intracellular copper concentration and attenuates Abeta-mediated neurotoxicity facilitated by the addition of copper in the hippocampus and cortex of APP(V717I) (London mutant form of APP) transgenic mice.

Pathology Alzheimer Show Other

Stage Late Show Other

Question Exclude - biochemistry

Claim