Alzheimer Video News

Oklahoma mother and daughter discuss one year sustained results with perispinal etanercept

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Mother and daughter have been flying from Oklahoma to Los Angeles for one year for perispinal etanercept anti-TNF treatment at the INR® Los Angeles.

Please visit the website of the INR® for further information at www.nrimed.com.

Etanercept reaches cerebrospinal fluid in animal model

Rapid intracerebroventricular delivery of 64Cu-DOTA-etanercept after peripheral administration demonstrated by PET imaging

Edward L Tobinick, Kai Chen and Xiaoyuan Chen

BMC Research Notes 2009, 2:28
Published:     27 February 2009

Abstract 

Background

The cytokines interleukin-1 and tumor necrosis factor (TNF), and the cytokine blocker interleukin-1 receptor antagonist, all have been demonstrated to enter the cerebrospinal fluid (CSF) following peripheral administration. Recent reports of rapid clinical improvement in patients with Alzheimer's disease and related forms of dementia following perispinal administration of etanercept, a TNF antagonist, suggest that etanercept also has the ability to reach the brain CSF. To investigate, etanercept was labeled with a positron emitter to enable visualization of its intracranial distribution following peripheral administration by PET in an animal model.

Findings

Radiolabeling of etanercept with the PET emitter 64Cu was performed by DOTA (1,4,7,10-tetraazadodecane-N,N',N'',N'''-tetraacetic acid) conjugation of etanercept, followed by column purification and 64Cu labeling. MicroPET imaging revealed accumulation of 64Cu-DOTA-etanercept within the lateral and third cerebral ventricles within minutes of peripheral perispinal administration in a normal rat anesthesized with isoflurane anesthesia, with concentration within the choroid plexus and into the CSF.

Conclusions

Synthesis of 64Cu-DOTA-etanercept enabled visualization of its intracranial distribution by microPET imaging. MicroPET imaging documented rapid accumulation of 64Cu-DOTA-etanercept within the choroid plexus and the cerebrospinal fluid within the cerebral ventricles of a living rat after peripheral administration. Further study of the effects of etanercept and TNF at the level of the choroid plexus may yield valuable insights into the pathogenesis of Alzheimer's disease.

Read the abstract and full article at Biomed Central Research Notes

Targeting Alzheimer's with Novel Therapeutics

Cambridge Healthtech Institute's Eighth Annual
World Pharmaceutical Congress
June 10-11, 2009   Philadelphia, PA

Cambridge Healthtech Institute's 8th annual World Pharmaceutical Congress takes place in Philadelphia this year and will feature the inaugural Targeting Alzheimer's with Novel Therapeutics conference from June 10-11.

This inaugural Alzheimer's conference features the leading developers of cutting edge therapeutics for Alzheimer's disease, including perispinal etanercept, Rember™, and Dimebon™.

Edward Tobinick, M.D., Director of the Institute for Neurological Research®, a private medical group, inc.(INR®) will present TNF Modulation for Treatment of Alzheimer's Disease, a discussion of the use of perispinal etanercept for Alzheimer's and related forms of dementia.

Claude M. Wischik, Ph.D., Professor Old Age Psychiatry University of Aberdeen and Chairman TauRx Therapeutics will present Potential Efficacy of Tau Aggregation Inhibitor Therapy with Rember™ in Alzheimer's Disease and

Dimebon: Turning an Old Drug to a New Use will be presented by Lynn Seely, M.D., Chief Medical Officer, Medivation, Inc.

Holding promise are Rember™ and Dimebon™ which are experimental drugs not presently available to the public for therapeutic use.  Perispinal etanercept, a unique, patented[1] immunomodulatory approach developed by Dr. Tobinick at the INR®, is currently available to patients at the INR® Los Angeles and from INR trained physicians in North America, Europe and Africa.

The major pharmaceutical giants also searching for a treatment for the over 5 million Americans suffering from Alzheimer's disease will be represented at the Targeting Alzheimer's with Novel Therapeutics conference by:

Chairperson Timothy A. Esbenshade, Ph.D., Senior Group Leader, Neuroscience Research, Abbott Laboratories

Scott D. Bembenek, Ph.D.,  Senior Scientist, Computer Aided Drug Discovery, Johnson & Johnson

Michael L. Hutton, Ph.D., Leader, Alzheimer's Group, Merck Research Laboratories

For further information, please visit:

Institute for Neurological Research, a private medical group, inc.  Los Angeles, California website

World Pharmaceutical Congress

[1] Multiple issued and pending U.S. and international patents, including, but not limited to, US patents 6,982,089 and 7,214,658.

Children discuss improvement after perispinal etanercept for Alzheimer's

Daughters discuss improvement over the past year in quality of life and care management for their mother with severe dementia after perispinal etanercept administration at the Institute for Neurological Research®, a private medical group, inc. in Los Angeles.

Novelist Terry Pratchett on world wide quest for Alzheimer's treatment

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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.

Watch the Speech by Terry Pratchett

Excess TNF implicated in additional brain disorders

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excerpts:

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].

Increasing scientific evidence supports an anti-TNF approach In Alzheimer's disease

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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