Pathological mechanism

Data

Name Memantine reduces APP, Galantamine and Nicotine increase synaptophysin

Description

Hypothesis LTP hypothesis Show Other

Extracelular pathological element

Intracelular pathological element

Pathological action Reduces Show Other

Process

Process action

Transmitter(s)

Receptor(s) NMDA Show Other

Channel(s)

Pharmacological Agent

Pharmacological Action

Brain region

Neuron

Cell model

Cellular compartment

PubMed ID 16354790

Citation Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain. Show Other

AlzWeb

Notes Effect of subchronic treatment of memantine, galantamine, and nicotine in the brain of Tg2576 (APPswe) transgenic mice.Unger C, Svedberg MM, Yu WF, Hedberg MM, Nordberg A. J Pharmacol Exp Ther. 2006 Apr;317(1):30-6. Memantine treatment reduced the total cortical levels of membrane-bound amyloid precursor protein (45-55%) in both transgenic and nontransgenic mice, which eventually may decrease the level of Abeta.Treatment with nicotine also resulted in less glial fibrillary acidic protein immunoreactive astrocytes around the plaques, increased levels of synaptophysin, and increased number of alpha7 nicotinic acetylcholine receptors (nAChRs) in the cortex of APPswe transgenic mice. Galantamine treatment caused an increase in the cortical levels of synaptophysin in the APPswe mice.

Pathology Alzheimer Show Other

Stage Late Show Other

Question Exclude - biochemistry

Claim