Oxidative stress is implicated in the pathogenesis of different human diseases: Alzheimer, Parkinson,
Huntington, amyotrophic lateral sclerosis (Lou Gehrig's disease), Down’s syndrome, atherosclerosis, vascular disease,
cancer, diabetes mellitus type 1 and type 2, age – related macular degeneration, psoriatic arthritis. The aim of current
study is to summarize the scientific evidences for the antioxidant and neuroprotective activity of Galantamine and some of
its derivatives. Galantamine is a scavenger of reactive oxygen species and causes neuroprotective effect by lowering the
oxidative neuronal damage, through the following pathways: 1) prevention of the activation of P2X7 receptors; 2) protection
of mitochondrial membrane potential; 3) pre – vention of the membrane fluidity disturbances. Another mechanism is
the decreasing of the overproduction of reactive oxygen species, a result from the increasing of acetylcholine level due to:
1) acethylcholinesterase inhibition; 2) allosteric potentiation of α7 – subtype of nicotinic acetylcholine receptors. A close
relationship between acethylcholinesterase inhibition and reduced oxidative injury is observed. Through allosteric potentiation
of the α7 – subtype of nicotinic acetylcholine receptors, the drug leads to induction of phosphorylation of serine –
threonine protein kinase, stimulates phosphoinositide 3 – kinase and elevates the expression of protective protein Bcl – 2.
By activation of these important neuroprotective cascades, Galantamine exerts neuroprotection against a variety of cytotoxic
agents (β – amyloid peptide, glutamate, hydrogen peroxide, oxygen and glucose deprivation). The new trend in therapy
of Alzheimer's disease will be the investigation and application of compounds such as Galantamine derivatives, which
possess acethylcholinesterase and γ – secretase inhibitory activity and antioxidant properties.