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P2–404: Resistant depression in Alzheimer's disease(AD)
Author(s) -
Ciobanu Adela M.
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.1245
Subject(s) - clinical global impression , tolerability , hamd , depression (economics) , medicine , sertraline , carbamazepine , clinical endpoint , mini–mental state examination , hamilton depression scale , gastroenterology , adverse effect , psychiatry , clinical trial , disease , cognitive impairment , epilepsy , significant difference , antidepressant , placebo , alternative medicine , pathology , hippocampus , economics , macroeconomics
Background: Current pharmacologic treatment for Alzheimer’s Disease(AD) is unable to prevent long-term clinical deterioration. TNF-alpha, a proinflammatory cytokine, has been implicated in the pathogenesis of AD. We investigated the use of a biologic TNF inhibitor, etanercept, for mild to severe AD, given by perispinal extrathecal administration. Objective(s): To explore the feasibility of the use of a biologic TNF inhibitor, etanercept, given by perispinal extrathecal administration, for treatment of Alzheimer’s Disease. Methods: Patients were treated open-label with perispinal extrathecal etanercept, with a total weekly dose ranging from 25mg to 50mg. The primary efficacy variables were the change from baseline in three standard measures of cognition: the MMSE for all patients; the ADAS-Cog for patients with mild-moderate AD; and the Severe Impairment Battery (SIB) for patients with more severe AD. 15 patients were treated and evaluated through six months. Results: The average age was 76.7. The mean baseline MMSE was 18.2 (n 15); the mean baseline ADAS-Cog was 20.8 (n 11); the mean baseline SIB was 62.5 (n 5). There was significant improvement with treatment, as measured by all of the primary efficacy variables, through six months: MMSE increased by 2.13Â 2.23; ADAS-Cog improved(decreased) by 5.48Â 5.08; and SIB increased by 16.6Â 14.52. Conclusions: Increasing basic science and clinical evidence implicates excess TNF-alpha in the pathogenesis of Alzheimer’s Disease. This small, open-label pilot study suggests that TNF-alpha modulation may hold promise as a potential new treatment approach. Further study of perispinal extrathecal etanercept in randomized, placebo-controlled clinical trials is merited.