Selected recent Publications:
Edward Tobinick MD, Hyman Gross
MD.
Rapid cognitive
improvement in Alzheimer's disease following perispinal etanercept
administration.
J Neuroinflammation 2008 Jan 9; 5(1):2. [Download full-text PDF].
Edward Tobinick MD.
Perispinal
etanercept for treatment of Alzheimer's disease. [Link
to PubMed abstract]
Curr Alzheimer Res 2007 Dec;
4(5):550-2.
Edward Tobinick MD.
A critique
of intradiscal administration for treatment of radiculopathy.
Anesthesiology 2008 Feb; 108(2):334; author reply 335.
Edward Tobinick MD.
Correspondence:
Inflammatory markers and the risk of Alzheimer Disease: The Framingham
Study. Neurology 2007 August
20, correspondence.
Edward Tobinick MD.
Paradigm Shift:
Excess TNF-alpha emerges as a key therapeutic target in Alzheimer's
Disease. MedGenMed 2007
July 20; 9(3):17.
Edward Tobinick MD. Spinal Delivery of p38: TNF-alpha Inhibitors. PLoS Med 2006 Nov; 3(11) :e511.
Edward Tobinick MD, Hyman Gross
MD, Alan Weinberger MD, Hart Cohen MD FRCPC
TNF-alpha
Modulation for Treatment of Alzheimer's Disease: A 6-Month Pilot
Study. Alzheimer's and
Dementia 2006 July, 2(3), Supp. 1, Pages S364-5.
Edward Tobinick MD, Hyman Gross
MD, Alan Weinberger MD, Hart Cohen MD FRCPC
TNF-alpha
Modulation for Treatment of Alzheimer's Disease: A 6-Month Pilot
Study. MedGenMed 2006;
8(2) :25.
Edward Tobinick MD
The Cerebrospinal
Venous System: Anatomy, Physiology, and Clinical Implications.
MedGenMed 2006; 8(1) :53.
Edward Tobinick MD
TNF-alpha
inhibition for potential therapeutic modulation of SARS coronavirus
infection.
Curr Med Res Opin 2004
Jan; 20(1) :39-40.
Edward Tobinick MD
Targeted etanercept
for treatment-refractory pain due to bone metastasis: two case
reports.
Clin Ther 2003 Aug; 25(8)
:2279-88.
Links to abstracts and full-text:
TNF-alpha modulation for treatment of Alzheimer's Disease: A 6-month pilot study
The cerebrospinal venous system: anatomy, physiology, and clinical implications
Spinal delivery of p38:TNF-alpha inhibitors
Selected abstract:
Title:TNF-alpha Modulation for Treatment of Alzheimer's
Disease: A 6-Month Pilot Study.
Author(s): Tobinick E, Gross H, Weinberger
A, Cohen H.
Source: MedGenMed 2006; 8(2) :25., Abstract
Context: Current pharmacologic treatments for Alzheimer's disease
(AD) do not prevent long-term clinical deterioration. Tumor necrosis
factor (TNF)-alpha, a proinflammatory cytokine, has been implicated
in the pathogenesis of AD.
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: Increasing 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.
PubMed ID 16926764