3+ things that trigger Alzheimer’s plaques and tangles

Plaques and neurofibrillary tangles are like a stamp on the brain that may as well read “Alzheimer’s was here.”

They are the hallmark indicators of one of the most feared diseases of mankind.

But what exactly are these substances and why do they have the effect that they do on the brain?

I get these questions a lot, closely followed by… How do they get there? And can anything keep them away?

Let’s talk about that…

How plaques and tangles lead to Alzheimer’s

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 which causes 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.

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.

That means they could be doing their damage long before the symptoms start.

Causes behind the plaques and tangles

One reason I wanted to write on this subject this week is because of something I recently read about… Iatrogenic (treatment-induced) transmission of plaques and tangles.

Unfortunately, certain proteins called prions that stimulate abnormal beta-amyloid and tau proteins have been accidentally transmitted in human growth hormone (hGH) given to humans.

Related: Can Alzheimer’s dementia be reversed?

This recent discovery reported in the December 2018 issue of Nature and previously in the January 2018 issue of Acta Neuropathologica Communications, 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. 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.

Certainly alarming, but you should really be concerned about what else triggers beta-amyloid and tau protein build up that could be more likely to affect you…

Peak PS

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Other causes behind plaques and tangles of Alzheimer’s disease

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…

1. 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

2. Inflammation: Contributors to neurodegenerative inflammation include:

  • Unhealthy gut lining (leaky gut syndrome and the autoimmune toxicity that it can cause)
  • Xenobiotics (hormone mimickers)
  • Exposure to aluminum (found in many deodorants, antacids, anti-diarrhea medications, baking powder, and cookware)
  • Malnutrition
  • Head injury
  • Infections

3. 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, caused by:

  • Iron and copper (study authors suggest chelation therapy to remedy this)
  • Low vascular blood flow (atherosclerosis)
  • High homocysteine blood levels
  • 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 interventions

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.

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 post, I’ll cover the important details of the specific nutritional supplements that could slow the progression of dementia.

To excellent mental clarity and feeling good,

Editor’s note: While you’re doing all the right things to protect your brain as you age, make sure you don’t make the mistake 38 million Americans do every day — by taking a drug that robs them of an essential brain nutrient! Click here to discover the truth about the Cholesterol Super-Brain!

Michael Cutler, M.D.

Sources:

  1.  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.
  2.  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 hormoneNature. 2018 Dec;564(7736):415-419. PubMed PMID: 30546139.
  3. 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 studyActa Neuropathol Commun. 2018 Jan 8;6(1):5. PubMed PMID: 29310723.
  4. Fasano A. Leaky gut and autoimmune diseases — Clin Rev Allergy Immunol. 2012 Feb;42(1):71-8.
  5.  Walton JR. Aluminum involvement in the progression of Alzheimer’s disease —  J Alzheimers Dis. 2013 Jan 1;35(1):7-43.
  6.  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.
  7.  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.
  8.  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.
  9.  Armstrong RA. What causes Alzheimer’s disease? — Folia Neuropathol. 2013;51(3):169-188.
  10.  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.
  11.  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.
  12.  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.
  13.  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.
Dr. Michael Cutler

By Dr. Michael Cutler

Dr. Michael Cutler is a graduate of Tulane University School of Medicine and is a board-certified family physician with more than 20 years of experience. He serves as a medical liaison to alternative and traditional practicing physicians. His practice focuses on an integrative solution to health problems. Dr. Cutler is a sought-after speaker and lecturer on experiencing optimum health through natural medicines and founder of the original Easy Health Options™ newsletter — an advisory on natural healing therapies and nutrients. His current practice is San Diego Integrative Medicine, near San Diego, California.

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