Alzheimer’s Dementia update – part 2



In this article I’ll be looking at causes of Alzheimer’s dementia that you may not have expected. Also, a look at what causes Alzheimer’s to develop, which will set the stage to be able to understanding how specific nutrient supplements can slow the progression of dementia.


To better understand how nutrient supplements can slow the progression of dementia, we must first know a little about what is seen under the microscope in the brain tissue of Alzheimer’s patients. We call them plaques and neurofibrillary tangles.


What are plaques and tangles?

Plaques are deposits of a “sticky” protein fragment called beta-amyloid that builds up in the synapses (space between nerve cells), thus blocking cell-to-cell signaling of the key neurotransmitter acetylcholine. This beta-amyloid protein build-up also activates immune system cells of inflammation, causing more damage.


Neurofibrillary tangles are aggregates of tau protein, which normally help stabilize the microtubular structure of nerve cell axons. However, when tau proteins dysfunction, they breakdown living cells by blocking nerve synapses. Tau proteins clump and stick together (to make tangles) which block vital nutrients and cause the cells to die.[1]


Interestingly, we do know from science released in 2012 that these abnormal proteins in the cerebral spinal fluid of individuals with Alzheimer’s disease can be found 16 years (on average) prior to noticeable memory loss or cognitive decline.[2]


Iatrogenic (treatment-induced) transmission of plaques and tangles

Unfortunately, prions (proteins) that stimulate abnormal beta amyloid and tau proteins have been accidentally transmitted in human growth hormone (hGH) given to humans. This recent discovery reported[3] in the December 2018 issue of Nature and previously[4] in the January 2018 issue of Acta Neuropathologica Cmmunications, shows us that surgeons and doctors have been unknowing inoculating recipients of human growth hormone (hGH) extracted from pituitary glands of human cadavers.


Human cadaver pituitary-derived growth hormone (hGH) apparently was contaminated with beta amyloid seeds as well as with prions. Prions are misfolded proteins that, under some conditions, can act as infectious agents. Therefore, up until the 1980s, people who had been treated during childhood with pituitary-derived growth hormone(c-hGH) from human cadavers contaminated with prions, developed Creutzfeld-Jacob disease. Creutzfeldt-Jakob disease is similar to and a more advanced form of Alzheimer’s, with dramatic amounts of brain beta amyloid and tau protein.


Other causes behind plaques and tangles of Alzheimer’s disease

Now you may ask, “what else triggers beta-amyloid and tau protein build up?”


Genetic predisposition plays a role for sure. Add such genetic predisposition to other factors (listed below) and you have a perfect recipe for Alzheimer’s to develop.


Small vessel (vascular) disease: this is a common condition in elderly people, known as atherosclerosis. It causes reduced blood flow and nutrient supply to the sensitive nerve tissue of the brain in aging Alzheimer’s patients. Consider risk factors for atherosclerosis, which include:

  • Uncontrolled hypertension

  • unhealthy diet

  • smoking

  • diabetes

  • obesity

  • sedentary lifestyle

  • high stress, and

  • low HDL-cholesterol blood levels

Inflammation: Contributors to neurodegenerative inflammation include

  • unhealthy gut lining[5] (leaky gut syndrome and the autoimmune toxicity that it can cause)

  • xenobiotics (hormone mimickers)

  • exposure to aluminum[6] [7] [8] [9](found in many deodorants, antacids, anti-diarrhea medications, baking powder, and cookware)

  • malnutrition

  • head injury

  • infections[10]

Oxidative stress is the microscopic process in which pro-oxidant molecules overwhelm antioxidant molecules. In Alzheimer’s dementia, oxidative stress occurs in mitochondria (energy and processing factories) of nerve cells,[11] caused by

  • iron and copper[12] (study[13] authors suggest chelation therapy to remedy this)

  • low vascular blood flow[14] (atherosclerosis)

  • high homocysteine blood levels[15]

  • smoking

  • excessive alcohol consumption

  • too many prescription medications

  • pesticides (on produce)

  • foods with artificial flavorings, preservatives and dyes

  • chemicals in personal care products (xenoestrogens)

  • high electromagnetic frequency (called EMF) exposure

Benefits of early natural treatments, not prescription drugs

There are many nutrient supplements shown to slow the progression of dementia. This is important because of the fact that synthetic prescription medications used for Alzheimer’s dementia may be modestly effective—but their effects are unfortunately short-lived; these prescription drugs typically only last 6-12 months while the underlying disease process of brain cell damage continues to progress. Moreover, only about half of the individuals who take prescription medications for Alzheimer’s get this benefit.

In my next and final article of this topic, you’ll learn the important details of the specific nutrient supplements that can slow the progression of dementia.


To excellent mental clarity and feeling good all our lives,


Michael Cutler, M.D.


____________________________

[1] “Alzheimer's Brain Tangles.” Alzheimer's Association, www.alz.org/braintour/tangles.asp

[2] Reiman EM, et al. Brain imaging and fluid biomarker analysis in young adults at genetic risk for autosomal dominant Alzheimer's disease in the presenilin 1 E280A kindred: a case-control study. Lancet Neurol Dec 2012; 11(12):1048-56. Read more online about this finding at: http://www.nytimes.com/2012/11/13/health/alzheimers-precursors-founds-at-earlier-age.html?_r=1&

[3] Purro SA, Farrow MA, Linehan J, Nazari T, Thomas DX, Chen Z, Mengel D, Saito T, Saido T, Rudge P, Brandner S, Walsh DM, Collinge J. Transmission of amyloid-β protein pathology from cadaveric pituitary growth hormone. Nature. 2018 Dec;564(7736):415-419. PubMed PMID: 30546139. https://www.ncbi.nlm.nih.gov/pubmed/30546139

[4] Cali I, Cohen ML, Haik S, Parchi P, Giaccone G, Collins SJ, Kofskey D, Wang H, McLean CA, Brandel JP, Privat N, Sazdovitch V, Duyckaerts C, Kitamoto T, Belay ED, Maddox RA, Tagliavini F, Pocchiari M, Leschek E, Appleby BS, Safar JG, Schonberger LB, Gambetti P. Iatrogenic Creutzfeldt-Jakob disease with Amyloid-β pathology: an international study. Acta Neuropathol Commun. 2018 Jan 8;6(1):5. PubMed PMID: 29310723. https://www.ncbi.nlm.nih.gov/pubmed/29310723

[5] Fasano A. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol. 2012 Feb;42(1):71-8.

[6] Walton JR. Aluminum involvement in the progression of Alzheimer's disease. J Alzheimers Dis. 2013 Jan 1;35(1):7-43.

[7] Shaw CA, Tomljenovic L. Aluminum in the central nervous system (CNS): toxicity in humans and animals, vaccine adjuvants, and autoimmunity. Immunol Res. 2013 Jul;56(2-3):304-16.

[8] Bhattacharjee S, Zhao Y, Hill JM, Culicchia F, Kruck TP, Percy ME, Pogue AI, Walton JR, Lukiw WJ.

Selective accumulation of aluminum in cerebral arteries in Alzheimer's disease (AD). J Inorg Biochem. 2013 Sep;126:35-7.

[9] Yokel RA. Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration. J Alzheimers Dis. 2006 Nov;10(2-3):223-53.

[10] Armstrong RA. What causes alzheimer's disease? Folia Neuropathol. 2013;51(3):169-188.

[11] Forero DA, Casadesus G, Perry G, Arboleda H. Synaptic dysfunction and oxidative stress in Alzheimer's disease: emerging mechanisms. J Cell Mol Med. 2006 Jul-Sep;10(3):796-805.

[12] Zhu X, Su B, Wang X, Smith MA, Perry G. Causes of oxidative stress in Alzheimer disease. Cell Mol Life Sci. 2007 Sep;64(17):2202-10.

[13] Smith MA, Nunomura A, Zhu X, Takeda A, Perry G. Metabolic, metallic, and mitotic sources of oxidative stress in Alzheimer disease. Antioxid Redox Signal. 2000 Fall;2(3):413-20.

[14] Zhu X, Su B, Wang X, Smith MA, Perry G. Causes of oxidative stress in Alzheimer disease. Cell Mol Life Sci. 2007 Sep;64(17):2202-10.

[15] Ibid.

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