Pathological mechanism

Data

Name Nicotine decreases intracellular Cu+2 concentration. Abeta increases.

Description

Hypothesis Nicotinic Receptor Hypothesis Show Other

Extracelular pathological element beta Amyloid Show Other

Intracelular pathological element Copper Show Other

Pathological action Increases Show Other

Process

Process action

Transmitter(s)

Receptor(s)

Channel(s)

Pharmacological Agent Nicotine Show Other

Pharmacological Action Opposes Show Other

Brain region Hippocampus CA1 Show Other

Neuron

Cell model

Cellular compartment

PubMed ID 16627626

Citation

AlzWeb

Notes A significant reduction in the metal contents of copper and zinc in senile plaques and neuropil is observed after nicotine treatment in the hippocampus and cortex of APP(V717I) (London mutant form of APP) transgenic mice.Nicotine treatment decreases the intracellular copper concentration and attenuates Abeta-mediated neurotoxicity facilitated by the addition of copper, and these effects are independent of the activation of nicotinic acetylcholine-receptor. Nicotine attenuates beta-amyloid-induced neurotoxicity by regulating metal homeostasis.Zhang J, Liu Q, Chen Q, Liu NQ, Li FL, Lu ZB, Qin C, Zhu H, Huang YY, He W, Zhao BL.FASEB J. 2006 Jun;20(8):1212-4.

Pathology Alzheimer Show Other

Stage Late Show Other

Question Exclude - biochemistry

Claim