Substantial evidence now exists that oxidative stress may play an important
role in the etiopathogenesis of DAT. The different sources of oxidative st
ress in DAT are suggesting several pharmacological opportunities for influe
ncing the disease. It is possible to distinguish 2 major types of possible
therapeutic agents according to their pharmacological. point of attack.
1. Radical scavengers, agents directly interacting with free radicals. Cand
idates of this type are gingko biloba, vitamins A, C, E and estrogen.
2. Antioxidants, which are able to prevent or decrease the production of fr
ee radicals by use of specific neuropharmacological properties. Candidates
are selegiline, a MAO-B inhibitor well established in the therapy of Parkin
son's disease, and tenilsetam, which is believed to be an AGE-inhibitor.
Recent in vitro studies have demonstrated the efficacy of both types of the
rapeutic agents by preventing or delaying oxidative neural damage.
Some clinical data exist regarding the antidementive properties particularl
y in terms of gingko biloba, selegiline and vitamin E. The efficacy studies
about these compounds seem to indicate a promising future strategy in the
therapy of DAT. But it is too early to draw definite conclusions since it i
s well kown that all of our candidate substances do not act specifically as
radical scavengers or antioxidants.