AEIF Newsletter 7: Present and Future Protocols for Treatment and Intervention
For more than a century, the treatment of Alzheimer's Disease (AD) has remained elusive, as no pathogen or vector has been identified. However, our updated understanding of the pathogenesis should provide a clearer pathway to understanding the various conduits of exposure and potential methods of treatment. In this process of identification, early detection is imperative for effective therapeutic intervention and potential discovery of the vectors and/or pathogens. To that end, Dr. Maria Carrillo, Chief Scientific Officer of the Alzheimer’s Association, spoke at the Time 100 Health Summit in October 2019, strongly recommending “cognitive assessments as a part of routine annual healthcare”. Development of and reference to a reproducible baseline Mild Cognitive Impairment (MCI) exam is imperative to this process of early detection, intervention, and standardized future productive investigations.
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Categories of Present Care:
Key features of this disease include early loss of smell and taste, MCI, abnormal development of increasing cerebrospinal fluid (CSF), tau and beta amyloid sticky proteins and traces of microscopic aluminum particles embedded in the neurofibrillary tangles (NFTs).12 There are drug and non-drug therapy options that may facilitate treatment while improving quality of life for those afflicted by A.D. Treatments have developed for improving memory, behavior, inflammatory response, and nutrition, but none yet targeting the root cause of AD. There are a number of key critical aspects of early detection which are readily available and cost effective; smell impairment7, cognitive impairment, Central Auditory Processing disruption9, chemical and CSF blood tests8, decreased optical performance6 and olfactory event evoked responses2. Because of the escalating prevalence of Alzheimer’s Disease, it is essential that annual physical exams for persons aged 65 and older include baseline testing for these components. (See AEIF Newsletter 6)
Treatment must be geared toward the early pathogenic development of this disease. Progressive damage to the nervous system is marked by the initial loss of taste and smell, and insidious, painless form of meningoencephalitis. Microscopic particles of the heavy metal aluminum are unlikely to be ingested, but rather likely inhaled through the nasal cavity, possibly invading through a disrupted Blood Brain Barrier and/or traversing into perineural space, eventually embedding into the neurofibrillary tangles (See AEIF Newsletter 5, Figure 3).4 Beta-amyloid PET-CT exams have documented evidence of meningoencephalitis, observed in the base of the frontal lobe (olfactory cortex) and in the region of the anterior commissure and CSF. Scientific research substantiates the idea that beta amyloid adheres to the cortex symmetrically and bilaterally, causing progressive cortical atrophy and ventricular ependymal enlargement. Interference with neuronal synapses and interstitial metabolic processes has been implicated in this process of brain tissue liquefaction and neurolysis.10The interruption of the production, the interactions of these sticky proteins with the brain and their removal are the emphasis of present scientific pursuits.
Works Cited
1. Arendash, G. “A Clinical Trial of Transcranial Electromagnetic Treatment in Alzheimer’s Disease: Cognitive Enhancement and Associated Changes in CSF, Blood, and Brain Imaging.” Journal of Alzheimer’s Disease, Vol 71: 57-82. TEMT Clinical Trial in AD Patients
2. Murphy, Claire. “Loss of Olfactory Function in Patients with Alzheimer’s Disease. Springer Link.
3. Zetterberg, Henrik, et al. “Cerebrospinal Fluid Analysis Should Be Considered in Patients with Cognitive Problems.” International Journal of Alzheimer's Disease, vol. 2010, 2010, pp. 1–4., doi:10.4061/2010/163065.
4. Rey, Nolwen L., et al. “The Olfactory Bulb as the Entry Site for Prion-like Propagation in Neurodegenerative Diseases.” Neurobiology of Disease, vol. 109, 2018, pp. 226–248., doi:10.1016/j.nbd.2016.12.013.
5. Essig, Marko. Santos, Vasco. Schonknecht, Peter. Schroder, Johannes. Thomann, Philipp A. Toro, Pablo. “Reduced Olfactory bulb and tract volume in early Alzheimer’s disease-A MRI Study.” Neurobiology of Aging, Volume 30, Issue 5, May 2009, Pages 838-84. https://doi.org/10.1016/j.neurobiolaging.2007.08.001.
6. Brenton, Jonathan. “Visual and Ocular Manifestations of Alzheimer’s Disease and Their Use as Biomarkers for Diagnosis and Progression”. 2016.
7. Fisher, Kim. “Olfactory Dysfunction as a Global Biomarker for Sniffing out Alzheimer’s Disease: A Meta-Analysis” June 2018.
8. Madhusoodanan, J. “A Blood Test for Alzheimer’s Disease Draws Near”. January 14, 2019.
9. Gates, George A. “CENTRAL AUDITORY DYSFUNCTION AS A HARBINGER OF ALZHEIMER’S DEMENTIA”. September 12, 2011.
10. Hossain, Amir. “Amyloid Beta (Aβ) and Oxidative Stress: Progression of Alzheimer’s Disease”. November 11, 2018.
11. Caruso, Arturo. “Hydrogen peroxide and viral infections: A literature review with research hypothesis definition in relation to the current covid-19 pandemic”. November 2020.
12. Goldman, Bruce. “Scientists Reveal How Beta-Amyloid May Cause Alzheimer’s”. Stanford Medicine. September 19, 2013.
13. Chen, Angus. “The FDA is Reviewing Biogen’s ‘Breakthrough Alzheimer’s Treatment”. Newsbreak. August 8, 2020.
14. Lovelace Jr., Berkeley. “Biogen Stock Jumps 42% After FDA Staff Says It Has Enough Data to Support Approving Alzheimer’s Drug”. CNBC. November 4, 2020. 15. Agamanolis, Dimitri P. “The Normal CSF”. Neuropathology. April 2020.