[HTML][HTML] TNF-alpha modulation for treatment of Alzheimer's disease: a 6-month pilot study
E Tobinick, H Gross, A Weinberger… - Medscape General …, 2006 - ncbi.nlm.nih.gov
E Tobinick, H Gross, A Weinberger, H Cohen
Medscape General Medicine, 2006•ncbi.nlm.nih.govObjective To investigate the use of a biologic TNF-alpha inhibitor, etanercept was given by
perispinal extrathecal administration for the treatment of AD. Methods This was a
prospective, single-center, open-label, pilot (proof-of-concept) study, in which 15 patients
with mild-to-severe AD were treated for 6 months. We administered etanercept, 25-50 mg,
once weekly by perispinal administration. Main outcome measures included the Mini-Mental
State Examination (MMSE), the Alzheimer's Disease Assessment Scale-Cognitive subscale …
perispinal extrathecal administration for the treatment of AD. Methods This was a
prospective, single-center, open-label, pilot (proof-of-concept) study, in which 15 patients
with mild-to-severe AD were treated for 6 months. We administered etanercept, 25-50 mg,
once weekly by perispinal administration. Main outcome measures included the Mini-Mental
State Examination (MMSE), the Alzheimer's Disease Assessment Scale-Cognitive subscale …
Objective
To investigate the use of a biologic TNF-alpha inhibitor, etanercept was given by perispinal extrathecal administration for the treatment of AD.
Methods
This was a prospective, single-center, open-label, pilot (proof-of-concept) study, in which 15 patients with mild-to-severe AD were treated for 6 months. We administered etanercept, 25-50 mg, once weekly by perispinal administration. Main outcome measures included the Mini-Mental State Examination (MMSE), the Alzheimer's Disease Assessment Scale-Cognitive subscale (ADAS-Cog), and the Severe Impairment Battery (SIB).
Results
The average age of our patient population was 76.7. The mean baseline MMSE was 18.2 (n= 15); the mean baseline ADAS-Cog was 20.8 (n= 11); and 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 6 months: MMSE increased by 2.13±2.23, ADAS-Cog improved (decreased) by 5.48±5.08, and SIB increased by 16.6±14.52.
Conclusion
An increasing amount of basic science and clinical evidence implicates inflammatory processes and resulting glial activation in the pathogenesis of AD. This small, open-label pilot study suggests that inhibition of the inflammatory cytokine TNF-alpha may hold promise as a potential approach to AD treatment. Further study in randomized, placebo-controlled clinical trials is merited.
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