disturbance that could lead to an unfavorable outcome in any brain function, affecting the general welfare of the patient. P3-373 MILD COGNITIVE DISORDER AND DEPRESSION: TREATMENT WITH ASSOCIATION BETWEEN GALANTAMINE AND ESCITALOPRAM Julio Zarra 1 , Luisa Schmidt 2 , 1 Hospital Italiano de La Plata, La Plata, Argentina; 2 Centro M edico San Lucas, Gualeguaych u, Argentina. Background: During the past decade, there has been a growing interest in the predementia phase of these conditions because of suggestions that we may be able to identify the earliest clinical features of these illnesses before functional impairment is evident. Toward this end, the construct of mild cog- nitive impairment (MCI) has evolved to capture this predementia phase of cognitive dysfunction.Most investigators believe that if we wait for func- tional impairment and perhaps even mild cognitive symptoms to emerge, it may be too late to treat the underlying disease process. We would like to be able to prevent or postpone the disease process by intervening early. As such, the construct of MCI serves a useful purpose as a clinical stage in which meaningful interventions can take place. MCI may be an interme- diate step on the way to primary prevention, but it remains important for for- mulating research hypotheses. To evaluate the efficacy of galantamine and escitalopram association in patients with Mild Cognitive Disorder and De- pression. So there is a possible relation between the deficit in executive and cognitive cerebral function and depression or relation between the serotonin system and cholinergic system in relation with disease comorbidity cogni- tive-depression.To evaluate the therapeutic response in patients with comor- bility between mild cognitive disorder and depression in treatment with galantamine with escitalopram and the two drugs associated. Methods: A group of 705 patients with symptoms of mild cognitive disorder and depres- sion (DSM IV-TR) were separated in 3 groups of 235 patients. Each group received different treatment in 12 months: Group 1: galantamine 16 mg/ day.Group 2: escitalopram 10 mg/day.Group 3: Both drugs, same dose. Re- sults: The therapeutic response evaluated in HAM-D, M.A.D.R.S., M.M.S.E. and G.C.I. scores during 12 months. In the third group who re- ceived the two drugs associated, had much better response than the others and “brain enhancer.” Conclusions: The group who received the association of the cholinergic agent galantamine with antidepressant escitalopram had a relevant satisfactory therapeutic response: the best result, so there is a pos- sible relation between the deficit in cholinergic systems and depression. Dis- cussion: Could be cerebral cholinergic systems deficit a generator of depressive disorder? P3-374 TREATMENT BY ADDITION IN ALZHEIMER’S DISEASE: RATIONALE FOR COMBINATION THERAPY WITH GALANTAMINE AND MEMANTINE—EFFICACY AND SAFETY Julio Zarra, Luisa Schmidt, Centro de Neurolog ıa y Psiquiatr  ıa-Psicolog ıa, Gualeguaych u, Argentina. Background: Alzheimer’s has no current cure, but treatments for symptoms are available and research continues. Although current Alzheimer’s treat- ments cannot stop Alzheimer’s from progressing, they can temporarily slow the worsening of symptoms and improve quality of life for those with Alzheimer’s and their caregivers. Today, there is a worldwide effort un- der way to find better ways to treat the disease, delay its onset, and prevent it from developing.Considering the moderate clinical state the Alzheimer’s disease, without therapeutic response or poor therapeutic response with an anti dementia agent, we try improvement the therapeutic response with 2 drugs association. The efficacy, safety, and tolerability of cholinergic agent: galantamine and moderate affinity NMDA-receptor antagonist: memantine, were assessed taking into account the profile of patients with neurocognitive disorder: Alzheimer’s disease, from the clinical aspects and the different classifications. Methods: The experience included 428 patients who were enrolled in a prospective, observational, multicenter, and open-label study to receive 16 mg/day of galantamine and 30 mg/day of memantine for 12 months of treatment of addition. Results: The therapeutic response was measured using the mini-mental state examination (MMSE), Clinical De- mentia Rating (CDR), Alzheimer’s Disease Assessment Scale (ADAS- GOG), Functional Activities Questionnaire (FAQ) the Clinical Global Impression Scale (CGI) and the UKU scale of adverse effects.Taking into account the efficacy, safety and adverse events of the treatment, the final re- sults of the study showed that galantamine with addition memantine im- prove cognition, behavioural symptoms, and the general well-being of patients with cognitive impairment: Alzheimer’s disease. The incidence of adverse events was not significant and a very good profile of tolerability and safety was observed. Conclusions: At the conclusion of this session, we should be able to demonstrate with use the association memantine - galatamine in neurocognitive disorder: Alzheimer’s disease, improve cognition, behavioural symptoms, and the general state recognized as neuro- cognitive disorder. Discussion: Suggest that before Alzheimer’s disease continues evolution to a severe state, the pharmacological use this associa- tion to slowing or stopping the dementia process. P3-375 A MULTIDIMENSIONAL EFFECT-SIZE ANALYSIS OF CHOLINESTERASE INHIBITORS FOR ALZHEIMER’S DISEASE Kevin Peters, Jaclyn Orsetto, Trent University, Peterborough, Ontario, Canada. Background: The purpose of this study was to compute several different ef- fect size indices on the same set of cholinesterase inhibitor (ChEI) trials in Alzheimer’s disease (AD) in an effort to better evaluate the clinical signif- icance of these drugs, and to underscore the usefulness adopting a multidi- mensional effect size approach in this field. Methods: The present study is a secondary analysis of the Cochrane Systematic Review published by Birks (2006). The following effect size measures were computed: (1) the magni- tude of difference between drug and placebo groups on the ADAS-Cog was assessed using Cohen’s D; (2) the number of patients needed to treat (NNT) to get one improvement on the Clinician’s Interview-Based Impression of Change (CIBIC-Plus); (3) the number of patients needed to treat to get one patient to withdraw from a study due to an adverse event (the number needed to harm or NNH); and (4) the area under the curve (AUC) was cal- culated for the CIBIC-Plus and for the number of patients who withdrew due to an adverse event. The AUC estimates the probability that if you sampled 1 patient from the drug group and 1 from the placebo group, the outcome of the patient from the drug group would be better, or worse, than that of the patient in the placebo group. We examined the 8 studies reported in Birks (2006) for which data were available to compute all of these effect size in- dices. Results: The average Cohen’s D value was 0.37, suggesting a small benefit of the ChEIs on cognition. In terms of improvement on the CIBIC- Plus, the NNT was 13, but the AUC was only .54. With respect to the number of withdrawals due to an adverse event, the NNH was 8 and the AUC was .57. Conclusions: Although Cohen’s D suggested some benefit of the ChEIs at the group-level, effect size indices that provide information at the patient- level (i.e., NNT, NNH, AUC) suggested no benefit or even some harm associated with the ChEIs. These results underscore the need to consider multiple effect size indices when evaluating the clinical significance of a particular treatment. P3-376 ADVANCEMENT OFA DRUG-DISEASE TRIAL MODEL FOR ALZHEIMER’S DISEASE THROUGH A REGULATORY SCIENCE PATH: THE CAMD EXPERIENCE Klaus Romero 1 , Diane Stephenson 1 , James Rogers 2 , Dan Polhamus 2 , Kaori Ito 3 , Ruolun Qiu 3 , Brian Corrigan 4 , 1 Critical Path Institute, Tucson, Arizona, United States; 2 Metrum Research Group, Tariffville, Connecticut, United States; 3 Pfizer Inc., New London, Connecticut, United States; 4 Pfizer, New London, Connecticut, United States. Background: Recent failures of therapeutic candidates for Alzheimer’s dis- ease (AD) underscore the critical need for innovative approaches, including Poster Presentations: P3 P587