91 Shaywitz and Sbaywitz92 suggest that, in line with findings from animal studies, estrogen may be most effective during initial use. For example, Mulnard et al91 found that estrogen-treated AD patients exhibited significantly higher scores on the MMSE relative to placebo after 8 weeks, although no difference between the groups was observed after 1 year of treatment. While there are not yet sufficient data to reach a Inhibitors,research,lifescience,medical definitive conclusion regarding the merits of ERT for improving or stabilizing the cognitive symptoms of AD patients, estrogen may be effective in preventing or delaying

the onset, of dementia. Neuronal degeneration Neuronal degeneration is a central feature of AD, Inhibitors,research,lifescience,medical with cell loss occurring throughout the brain, but most, dramatically in association cortex, medial temporal lobes, and hippocampus. Thus, neurotrophic factors that might, preserve and stimulate neuronal

development have received increasing interest. Several investigators suggest that nerve growth factor (NGF) might be valuable for the treatment of AD, but, its inability to cross the blood-brain barrier has posed difficulties for this approach.93 Research has focused on the use of agents that www.selleckchem.com/products/R406.html appear to stimulate Inhibitors,research,lifescience,medical NGF production in the brain, such as idebenone. One of the first double-blind, multisite clinical trials to employ this agent in AD patients found that patients

Inhibitors,research,lifescience,medical treated with idebenone for 12 months exhibited statistically significant, dose-dependent improvement, on the ADAS-Cog and its noncognitive counterpart subscale, ADAS-Noncog, as well as on the CGI-C and instrumental, activities of daily living (IADL) subscales.94 Further studies arc required before the efficacy Inhibitors,research,lifescience,medical of idebenone can be fully assessed. Nootropics are suggested to be neural stimulants that appear to augment neuronal function, including neurotransmitter release. However, clinical trials with two common nootropics, piracetam and pramiracetam have yielded mixed results in AD patients.95-97 As Flicker and GrimleyEvans98 conclude, the available evidence does not support the use of piracetam. in the treatment of people with dementia because effects were found predominantly on global impression crotamiton of change, but not on any of the more specific measures. Recently, there has been increased focus on Ccrebrolysin®, a porcine brain-derived peptide preparation, which has been suggested to have neurotropic activity.99 ‘The results of in vitro and in vivo studies suggest that Cerebrolysin® may reduce microglial, activation, thus reducing the extent of inflammation and accelerated neuronal death.100 Two recent placebo-controlled clinical trials found that, over a 4-week period, Cerebrolysin®-treated AD patients exhibited significant improvement on the ADAS-Cog, CGI-C, and the MMSE.