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.
Alzheimer Video News is not medical advice nor should be treated as such.
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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
"This work suggests that targeting this hormone system may
not be an effective approach to slowing the rate of Alzheimer's
disease progression," said study leader Dr. Jeff Sevigny of
Merck Research Laboratories in North Wales, Pennsylvania,in a
statement.
While the drug succeeded in boosting levels of IGF-1 by 73
percent after a year, it failed to keep the disease from
advancing. "This compound showed no clinical benefit in the
population we studied," Sevigny said in a telephone interview.
By Julie Steenhuysen
CHICAGO, Nov 17 (Reuters) - An experimental Merck & Co Inc
drug that raises levels of a natural growth hormone
failed to improve memory skills in people with mild to moderate
Alzheimer's disease, U.S. researchers said on Monday.
The compound, called MK-677, stimulates the release of
insulin-like growth factor 1, or IGF-1, which has been shown in
mice to reduce levels of beta amyloid protein that forms sticky
plaques in the brain.
Merck spokesman Ian McConnell said the company has
discontinued research on the drug in Alzheimer's disease, but
studies in other conditions are still under way.
These plaques are a hallmark of Alzheimer's disease, a
progressive disease marked by memory loss, confusion and
eventually, the inability to care for oneself.
The study, published in the journal Neurology, was designed
to test whether age-related declines in levels of IGF-1 drive
the accumulation of amyloid beta in Alzheimer's patients, and
if restoring IGF-1 might help slow progression of the disease.
Scott+Scott LLP
Files Class Action Lawsuit Against Elan Corporation, plc On Behalf of
Investors -- ELN
NEW YORK, Nov. 13,
2008 (GLOBE NEWSWIRE) -- On November 13, 2008, Scott+Scott LLP filed a
class action lawsuit against Elan Corporation, plc (``Elan'' or the
''Company'') (NYSE:ELN - News) and certain officers and directors of the Company in
the U.S. District Court for the Southern District of New York. The
action is on behalf of those purchasing American Depository Receipts
(``ADRs'') of Elan during the period beginning June 17, 2008 through
July 29, 2008, inclusive (the ``Class Period''), for violations of the
Securities Exchange Act of 1934.
According to the complaint, during the Class Period,
Elan issued materially false and misleading statements regarding the
Phase II clinical results of the Company's investigational treatment
for Alzheimer's disease, bapineuzumab. As a result of defendants'
false statements and omissions during the Class Period, Elan ADRs
traded at artificially inflated prices.
Specifically, Elan failed to disclose unfavorable results from the
bapineuzumab trial in a June 17, 2008 press release regarding the
study, misrepresenting the safety and efficacy of the drug to
investors and analysts. As a result of the press release, Elan ADRs
surged upward nearly 11% in one day. However, when the detailed Phase
II results were finally disclosed, the Company's prior representations
on the safety and efficacy of bapineuzumab were shown to be overblown.
On that day, the price of Elan's ADRs plunged from $33.75 to
$19.63.
