Disclosure: Perispinal etanercept for Alzheimer's disease and other forms of dementia is a patented, off-label treatment method developed at the INR. U.S. patents 6,982,089 and 7,214,658, and additional issued and pending U.S. and foreign patents. These patents are assigned to TACT IP LLC.
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"There
is not a family in the land that hasn't been affected"
excerpts:
Accompanied by a BBC camera crew, Terry Pratchett visited the
INR
in Los Angeles on August 8th, 2008, to spend the day with Doctor Edward Tobinick, inventor of the novel anti-TNF approach to Alzheimer’s disease which has generated intense scientific interest in 2008.
It was reported that last month, Mr. Pratchett continued his quest by visiting the Prime Minister at 10 Downing Street to warn the Government that the UK faces a "Tsunami of Alzheimer's" disease unless research funding is increased. The purpose of the visit was to hand over a petition signed by 20,000 members of the public urging the Prime Minister to boost funds for the study of the disease.
Pratchett said he had received a positive response from politicians, but hopes to see more concrete action. "I've spoken to a lot of Alzheimer's experts around the world and they talk about a Tsunami of Alzheimer's over the next 20 years as the 'baby boomers' get old enough to be in line for the disease.
"Nearly everybody I have talked to around the country talks about
caring for their mother or father with the disease, so it seems there
is not a family in the land that hasn't been affected, yet it is like a
huge secret everybody shares."
"A comparatively small amount of money and action now will prevent an awful lot of terrible stress and expense in the decades to come."
The Alzheimer's Research Trust estimates that 700,000 people in the UK
are affected by dementia and related diseases - more than the total
number of cancer sufferers.
In this malaria study, TNF-alpha levels were found to be significantly elevated in the cerebrospinal fluid of children with cerebral malaria, in comparison with controls. The authors discussed the need for a selective, CNS-active, anti-TNF treatment modality.
Excess TNF-alpha has also been documented in traumatic brain injury[1], spinal cord injury[2-4], neuropathic pain[5, 6], frontotemporal dementia[7], sleep apnea[8], stroke[9, 10] and Alzheimer’s disease[11-15].
From AlzheimerVideoNews.com Los Angeles November 19, 2008
A new scientific report from China, published online ahead of print on November 1, 2008 in the journal Brain Research[1] is the latest in a series of new articles which support an anti-TNF approach for Alzheimer's disease. TNF stands for tumor necrosis factor-alpha, an immune molecule which is now known to regulate communication between brain cells. Excess TNF in the brain has previously been shown to occur in Alzheimer's disease, and to accompany disease progression.
The new genetic study from China, in which the presence of a gene which increased TNF production was associated with an increased risk of Alzheimer's disease, provides further support for an anti-TNF approach in AD. The authors of this study concluded: "The data suggest that inhibition of TNF-alpha protein production and activity might be a valuable therapeutic strategy for sporadic Alzheimer's disease."
The Brain Research report joins a series of new scientific articles which cite Dr. Tobinick's scientific publications in this field. This new series includes, in just the last few weeks, articles from researchers from the Stanford University School of Medicine[2]; the Brown University Geriatric Psychopharmacology Update[3], the Brain and Spinal Injury Center at the University of California San Francisco[4] and Neurology, Harvard University, Children's Hospital, Boston[4]; the Yale University School of Medicine[5]; the University of British Columbia[6]; the University of Texas Southwestern Medical Center at Dallas[7,9]; and the Center for Neural Development and Disease and the Department of Pharmacology and Physiology at the University of Rochester Medical Center[8].
For example, the researchers from the University of Rochester, in their article published October 30, 2008 in the American Journal of Pathology[8], state: "Data from our model suggest that a chronic inflammatory event mediated by TNF-alpha contributes to AD-related neuronal death and provides the rationale for developing TNF-alpha specific agents to subvert the disease process. Support for such an endeavor is preliminarily provided by a recently conducted open-label pilot study, where mild to severe AD patients were perispinally administered etanercept, a human TNFRII antagonist. After 6 months of treatment, a subset of patients exhibited cognitive improvement, suggesting that interfering with TNF-alpha mediated signaling can improve disease symptomatology."
It is apparent that there is increasing scientific interest in Dr. Tobinick's work with perispinal etanercept for Alzheimer's disease from academic medical centers from across the U.S. Perispinal etanercept is a patented* new approach to Alzheimer's disease which was developed at the Institute for Neurological Research®, a private medical group, inc. (INR®) in Los Angeles. Please visit the website of the INR® for further information, at www.nrimed.com.
The full-text of these articles is available online and their complete references are found below.
*U.S. patents 6,982,089; 7,214,658, and additional issued and pending patents assigned to TACT IP, LLC.
References:
1. Yang L, Lu R, Jiang L, Liu Z, Peng Y. Expression and genetic analysis of tumor necrosis factor-alpha (TNF-alpha) G-308A polymorphism in sporadic Alzheimer's disease in a Southern China population. Brain Res. 2008 Nov 1. [Epub ahead of print]. 2. Steinman, L., Nuanced roles of cytokines in three major human brain disorders. J Clin Invest, 2008. 118(11): p. 3557-63. 3. Brown University Geriatric Psychopharmacology Update, volume 12, number 10 October 2008 p. 4, International Conference on Alzheimer's Disease 2008: Summary of New Research: Perispinal Etanercept Improves Primary Progressive Aphasia. 4. Ferguson, A.R., R.N. Christensen, J.C. Gensel, B.A. Miller, et al., Cell death after spinal cord injury is exacerbated by rapid TNFalpha-induced trafficking of GluR2-lacking AMPARs to the plasma membrane. J Neurosci, 2008. 28(44): p. 11391-400. 5. van Dyck, C.H., Imaging microglial activation in Alzheimer's disease: what does it mean? Biol Psychiatry, 2008. 64(10): p. 833-4. 6. Schwab, C. and P.L. McGeer, Inflammatory aspects of Alzheimer disease and other neurodegenerative disorders. J Alzheimers Dis, 2008. 13(4): p. 359-69. 7. McCoy MK, Tansey MG. TNF signaling inhibition in the CNS: implications for normal brain function and neurodegenerative disease. J Neuroinflammation. 2008 Oct 17;5:45. 8. Janelsins, M.C., M.A. Mastrangelo, K.M. Park, K.L. Sudol, et al., Chronic Neuron-Specific Tumor Necrosis Factor-Alpha Expression Enhances the Local Inflammatory Environment Ultimately Leading to Neuronal Death in 3xTg-AD Mice. Am J Pathol, 2008 Oct 30. PMID:18974297. 9. McAlpine FE, Tansey MG. Neuroinflammation and tumor necrosis factor signaling in the pathophysiology of Alzheimer's disease. J Inflammation Res. 2008:I 29-39
"The successful animal model study is important to researchers because it gives preliminary data regarding the potential of this new therapeutic approach, which may have relevance to mechanisms of Alzheimer’s in humans. These results should be viewed conservatively, however, and only as an indicator for the design of subsequent human trials and not be extrapolated as necessarily working on the human brain at this point."
European Molecular Biology Organization Volume 9 Number 5 2008 by Howard Wolinsky
excerpts:
"The
super-detective Sherlock Holmes, invented by British author Sir Arthur
Conan Doyle (1859–1930), famously held that,"when you have eliminated
the impossible, whatever remains, however improbable, must be the
truth."
One might assume that this purely logical principle applies
equally well to new scientific ideas, given that scientists, like
Holmes, seek to uncover the truth. Ideally, a new hypothesis that helps
to explain previously unexplainable observations should therefore
replace previous theories.
Unfortunately, scientists do not always
follow a path of pure logic, as the German physicistMax Planck(1858–1947) once observed,"[a] new scientific truth does not triumph
by convincing its opponents and making them see the light, but rather
because its opponents eventually die, and a new generation grows up
that is familiar with it."
The
history of science is replete with theories that only became accepted
by the scientific community after a long and protracted uphill battle.Stanley Prusiner met a similar fate when he proposed that
proteins could be infectious agents; his prion theory, which won him
the Nobel Prize in Physiology or Medicine in 1997, needed many years
before it was accepted.
It
is not only the hypotheses that shatter well-established knowledge and
theories that are ridiculed, dismissed or rejected. Even a simple
insight—for example, that the bacterium Helicobacter pylori,
rather than physiological problems, causes stomach ulcers—is not always
quickly accepted. Australian physician Barry Marshall won some of the
most prestigious scientific prizes, including the Robert Koch and the
Lasker Prizes, before the clinical community grudgingly accepted that
he was right. For his insight, Marshall was eventually awarded the
Nobel Prize together with Robin Warren in 2005.
It is not only the
reluctance of established research fields and communities that slow
down the uptake of revolutionary hypotheses, but also a general
reluctance to explore new ideas and support those who do so.
"Many
of the novel uses of etanercept which Dr. Tobinick invented, beginning
nearly a decade ago, such as for sciatica, Alzheimer’s, and myasthenia
gravis, have subsequently been supported by peer-reviewed, published
studies performed by independent researchers from academic centers
across the globe[18-26].
"As an example, a recently completed,
double-blind, placebo-controlled study conducted by independent
researchers at Johns Hopkins/Walter Reed Army Medical Center has
confirmed the efficacy of etanercept for sciatica, using a patented,
perispinal method of administration of etanercept which Dr. Tobinick
invented[27]. "
Scientific references for this
presentation follow:
1. Tobinick, E., Perispinal etanercept for treatment of Alzheimer's disease. Curr Alzheimer Res, 2007. 4(5): p. 550-2. 2. Tobinick, E., H. Gross, A. Weinberger, and H. Cohen, TNF Modulation
for Treatment of Alzheimer's Disease: A 6-month Pilot Study. Medscape
General Medicine: Neurology, 2006. 8(2): p. 25f. 3. Tobinick, E.,
Perispinal Etanercept Produces Rapid Improvement in Primary Progressive
Aphasia: Identification of a Novel, Rapidly Reversible TNF-Mediated
Pathophysiologic Mechanism. Medscape Journal of Medicine, 2008. 10(6):
p. 135. 4. Tobinick, E.L. and H. Gross, Rapid improvement in
verbal fluency and aphasia following perispinal etanercept in
Alzheimer's disease. BMC Neurol, 2008. 8(1): p. 27. 5. Tobinick,
E.L. and H. Gross, Rapid cognitive improvement in Alzheimer's disease
following perispinal etanercept administration. J Neuroinflammation,
2008. 5: p. 2. 6. Tweedie, D., K. Sambamurti, and N.H. Greig,
TNF-alpha Inhibition as a Treatment Strategy for Neurodegenerative
Disorders: New Drug Candidates and Targets. Curr Alzheimer Res, 2007.
4(4): p. 375-8. 7. Tarkowski, E., N. Andreasen, A. Tarkowski, and
K. Blennow, Intrathecal inflammation precedes development of
Alzheimer's disease. J Neurol Neurosurg Psychiatry, 2003. 74(9): p.
1200-5.
