Alzheimer’s Disease
The INR Alzheimer Treatment Program – At last there is hope
There is widespread consensus within the Alzheimer research community that microscopic inflammation occurs in the Alzheimer brain[1-4]. The INR has developed a unique method designed to target this microscopic inflammation(glial activation) that is simply years ahead of its time. So far ahead that the results that may be seen are in a completely different class than those seen with the current drug treatments that are FDA-approved for Alzheimer’s. The INR Alzheimer treatment program is available for a select limited number of patients at the present time.
Inflammation and Alzheimer’s disease
There is substantial scientific support for the concept that the central cause of microscopic inflammation (glial activation) in the brain is elevation of an inflammatory molecule called TNF. TNF is present in the fluid surrounding the brain(the cerebrospinal fluid) at a level 25 times normal[3]. It is known that elevated TNF can interfere with neuronal function, a process that could interfere with normal communication (synaptic transmission) between brain cells[4-15]. The therapeutic molecule utilized at the INR, etanercept, is designed to directly bind to and instantaneously neutralize excess TNF. Etanercept is one of the most successful therapeutic agents in the world, with worldwide sales in excess of $7 billion per year and FDA-approved indications for rheumatoid arthritis, arthritis of the spine(anyklosing spondylitis), psoriasis(an inflammatory skin disease), arthritis associated with psoriasis, and juvenile arthritis in children.
The patented INR anti-TNF etanercept treatment program
Physicians have had more than 1.6 million patient-years of experience utilizing etanercept to treat their patients for the FDA-approved indications. The use of etanercept for the treatment of Alzheimer’s disease and other forms of dementia by local administration, a treatment method that is currently beyond the FDA-approved label(off-label), is a patented invention of the INR, and available exclusively at the INR and from INR trained and licensed physicians[4,19-23]. The scientific rationale for targeting TNF to treat Alzheimer’s disease is supported by studies performed by scientists at academic institutions around the world[1-18].
Please see the published, peer-reviewed scientific articles for a complete scientific explanation of the background of the INR treatment program[1-18]. The stories of the responses to treatment that may occur are illustrated by the videos present on this website. Although treatment results can vary these videos are of real INR patients and their families. The INR anti-TNF treatment program represents emerging medicine; breakthroughs in medicine that challenge existing paradigms often take years to be recognized[19, 20]. It would therefore seem fair to say that the average physician or neurologist would likely not be aware of the scientific basis, or even the existence, of the INR anti-TNF treatment program. Cutting edge science takes many years to be accepted, and even longer to become widely known(an average of 17 years, according to the National Institute of Medicine)[19, 20). The INR now has more than six years of experience with its anti-TNF treatment program, a program that is available at the INR, for Alzheimer patients and their families, today.
Become Our Patient
In order to determine if this treatment may be suitable for your family member, we first need to conduct a physician interview with the caregiver. We want to understand your family member's current condition, diagnosis, Alzheimer's medications as well as all other medications. Once we have a good picture of these areas, we can begin to determine if our treatment may be potentially suitable.
To get started, you can complete the form at this page. Fill it out, and one of our staff members will contact you to discuss your case further and to possibly arrange a consultation with one of INR's physicians. Or call the INR directly for more information, at (310) 824-6199.
References
- Inflammation and anti-inflammatory strategies for Alzheimer's disease--a mini-review. McNaull BB, Todd S, McGuinness B, Passmore AP. Gerontology. 2010;56(1):3-14.
- Systemic inflammation and disease progression in Alzheimer disease. Holmes C, Cunningham C, Zotova E, Woolford J, Dean C, Kerr S, Culliford D, Perry VH. Neurology. 2009 Sep 8;73(10):768-74.
- Intrathecal inflammation precedes development of Alzheimer's disease. Tarkowski E, Andreasen N, Tarkowski A, Blennow K. J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1200-5.
- Perispinal etanercept: a new therapeutic paradigm in neurology. Edward Tobinick MD. Expert Rev Neurother. 2010 Jun;10(6):985-1002.
- Tumour necrosis factor modulation for treatment of Alzheimer’s disease: rationale and current evidence. Edward Tobinick MD. CNS Drugs. 2009 Sep 1;23(9):713-25.
- Rapid intracerebroventricular delivery of Cu-DOTA-etanercept after peripheral administration demonstrated by PET imaging. Edward Tobinick MD, K Chen PhD, X Chen PhD. BMC Res Notes. 2009 Feb 27;2:28.
- Perispinal etanercept for neuroinflammatory disorders. Edward Tobinick MD. Drug Discov Today. 2009 Feb;14(3-4):168-77.
- Perispinal etanercept produces rapid improvement in primary progressive aphasia: identification of a novel, rapidly reversible TNF-mediated pathophysiologic mechanism. Edward Tobinick MD. Medscape J Med. 2008 Jun 10;10(6):135.
- Rapid improvement in verbal fluency and aphasia following perispinal etanercept in Alzheimer’s disease. Edward Tobinick MD, Hyman Gross MD. BMC Neurol. 2008 Jul 21;8:27.
- Perispinal etanercept for treatment of Alzheimer’s disease. Edward Tobinick MD. Curr Alzheimer Res. 2007 Dec;4(5):550-2.
- Rapid cognitive improvement in Alzheimer’s disease following perispinal etanercept administration. Edward Tobinick MD, Hyman Gross MD. J Neuroinflammation. 2008 Jan 9;5:2.
- TNF-alpha modulation for treatment of Alzheimer’s disease: a 6-month pilot study. Edward Tobinick MD, Hyman Gross MD, Alan Weinberger MD, Hart Cohen MD. MedGenMed. 2006 Apr 26;8(2):25.
- Perispinal etanercept: potential as an Alzheimer therapeutic.Griffin WS. J Neuroinflammation. 2008 Jan 10;5:3.
- Tumor necrosis factor-alpha mediated signaling in neuronal homeostasis and dysfunction. Park KM, Bowers WJ. Cell Signal. 2010 Jul;22(7):977-83.
- The roles of TNF in brain dysfunction and disease. Clark IA, Alleva LM, Vissel B. Pharmacol Ther. 2010 Sep 8, in press.
- An association study of 21 potential Alzheimer's disease risk genes in a Finnish population. Sarajärvi T, Helisalmi S, Antikainen L, et. al. J Alzheimers Dis. 2010;21(3):763-7.
- The role of TNF-alpha signaling pathway on COX-2 upregulation and cognitive decline induced by beta-amyloid peptide. Medeiros R, Figueiredo CP, Pandolfo P, et. al. Behav Brain Res. 2010 May 1;209(1):165-73.
- Soluble TNF receptors are associated with A? metabolism and conversion to dementia in subjects with mild cognitive impairment. Buchhave P, Zetterberg H, Blennow K, Minthon L, Janciauskiene S, Hansson O. Neurobiol Aging. 2010 Nov;31(11):1877-84.
- The U.S. National Institute of Medicine has established the lengthy time that it takes for a new treatment paradigm to be established, and this is codified in California law. See California B&P 2234.1(4c): "Since the National Institute of Medicine has reported that it can take up to 17 years for a new best practice to reach the average physician and surgeon, it is prudent to give attention to new developments not only in general medical care but in the actual treatment of specific diseases, particularly those that are not yet broadly recognized in California".
- Paths to acceptance. The advancement of scientific knowledge is an uphill struggle against 'accepted wisdom'. Wolinsky H. EMBO Rep. 2008 May;9(5):416-8.
- The off-label use of FDA-approved medications is both legal and a common occurrence in daily medical practice. Although drug manufacturers are prohibited from promoting off-label uses, physicians may and commonly use medications for off-label indications if there is an established scientific rationale. The scientific rationale for targeting TNF to treat Alzheimer’s disease is supported by studies performed by scientists at academic institutions around the world [see References 1-18 above].
- FDA, off-label use, and informed consent: debunking myths and misconceptions. Beck JM, Azari ED. Food Drug Law J. 1998;53(1):71-104.
- U.S. patents 6982089, 7214658, 7629311; Australian patent 758523; and additional pending and issued U.S. patents. These patents are assigned to TACT IP, LLC.