Category Archives: dementia

Rudolph Tanzi- Fight against Alzheimer’s Disease – amyloids

07 Friday Oct 2016

Posted by in aging, exercise, dementia, Uncategorized

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The cure for your infection, may be the thing that eventually kills you; amyloids which build up plaque in the brain associated with Alzheimer’s Disease. The brains reactive inflammation to the plaque may cause the onset of Alzheimer’s.

RESEARCH ARTICLEALZHEIMER’S DISEASE

Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer’s disease
  1. Deepak Kumar Vijaya Kumar1,*,
  2. Se Hoon Choi1,*,
  3. Kevin J. Washicosky1,*,
  4. William A. Eimer1,
  5. Stephanie Tucker1,
  6. Jessica Ghofrani1,
  7. Aaron Lefkowitz1,
  8. Gawain McColl2,
  9. Lee E. Goldstein3,
  10. Rudolph E. Tanzi1,† and
  11. Robert D. Moir1,†

+ ↵†Corresponding author. Email: moir@helix.mgh.harvard.edu (R.D.M.); tanzi@helix.mgh.harvard.edu (R.E.T.)

  • Science Translational Medicine  25 May 2016:

Vol. 8, Issue 340, pp. 340ra72
DOI: 10.1126/scitranslmed.aaf1059

Rehabilitation of a β-amyloid bad boy

A protein called Aβ is thought to cause neuronal death in Alzheimer’s disease (AD). Aβ forms insoluble aggregates in the brains of patients with AD, which are a hallmark of the disease. Aβ and its propensity for aggregation are widely viewed as intrinsically abnormal. However, in new work, Kumar et al. show that Aβ is a natural antibiotic that protects the brain from infection. Most surprisingly, Aβ aggregates trap and imprison bacterial pathogens. It remains unclear whether Aβ is fighting a real or falsely perceived infection in AD. However, in any case, these findings identify inflammatory pathways as potential new drug targets for treating AD.

Abstract

The amyloid-β peptide (Aβ) is a key protein in Alzheimer’s disease (AD) pathology. We previously reported in vitro evidence suggesting that Aβ is an antimicrobial peptide. We present in vivo data showing that Aβ expression protects against fungal and bacterial infections in mouse, nematode, and cell culture models of AD. We show that Aβ oligomerization, a behavior traditionally viewed as intrinsically pathological, may be necessary for the antimicrobial activities of the peptide. Collectively, our data are consistent with a model in which soluble Aβ oligomers first bind to microbial cell wall carbohydrates via a heparin-binding domain.  Consistent with our model, SalmonellaTyphimurium bacterial infection of the brains of mice resulted in rapid seeding and accelerated β-amyloid deposition, which (entrap invading bacteria). Our findings raise the intriguing possibility that β-amyloid may play a protective role in innate immunity and infectious or sterile inflammatory stimuli may drive amyloidosis. These data suggest a dual protective/damaging role for Aβ, as has been described for other antimicrobial peptides.

Dealing with Dementia – prevention and cures Drhyman.com

26 Monday Oct 2015

Posted by in dementia, diet

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Article taken from drhyman.com

There is no effective known treatment for dementia. But we do know a lot about what affects brain function and brain aging: our nutrition,inflammation, environmental toxins, stress, exercise, and deficiencies of hormones, vitamins, and omega-3 fats.

It is not just one gene, but the interaction between many genes and the environment that puts someone at risk for a chronic disease such as dementia. And we know that many things affect how our genes function — our diet, vitamins and minerals, toxins, allergens, stress, lack of sleep and exercise, and more.

Even though no long-term studies have been done to look at treating dementia based on genes, there are so many scientific threads that weave together a picture of how and why our brains age and what genes are involved. This leads me back to George …

For this man, whose mind and life were evaporating, I looked deeply into his genes and the biochemistry his genes controlled and found places where we could improve things.

He had a gene called apo E4, which is a high-risk gene for Alzheimer’s disease(ii) and also made it hard for him to lower his cholesterol anddetoxify mercury from his brain.(iii) He also had a version of a gene for detoxification of metals and other toxins (glutathione-S-transferase, or GST)(iv) that was very inefficient, making him accumulate more toxins over his lifetime. Having the combination of a problem with GST and apo E4 puts people at even more risk for dementia.(v),(vi) In another study, people with an absent GST gene were likely to have much higher levels of mercury.(vii)

George had another gene called MTHFR(viii) that made him require very high doses of folate to lower his blood levels of homocysteine, which is a substance very toxic to the brain. Lastly, he had a gene called CETP that caused his cholesterol to be high, which contributes to dementia. Combine this gene with the apo E4 gene and your risk of dementia goes way up.(ix)

We found that George had high levels of mercury(x) and helped him detoxify with foods such as kale, watercress, and cilantro, herbs such as milk thistle, nutrients such as selenium and zinc, and medications that helped him overcome his genetic difficulties by getting rid of toxins.

We lowered his cholesterol with diet and herbs. We lowered his homocysteine with high doses of folate and vitamins B6 and B12.

What happened then was impressive …

After a year of aggressive therapy that was matched to his genes, not his diagnosis, he had a remarkable and dramatic recovery. Before I saw him, he could not manage his business, nor did his grandchildren want to be around him.

While this area of genetic testing and nutrigenomics is new, and more research is needed to help us refine our understanding and treatment.

A woman named Christine was eighty and was experiencing severe memory loss and cognitive decline. Her family was obviously concerned, so she was tested with hours of neuropsychological testing and found to have dementia.

Her neurologist offered her words of comfort, but told her and her family there is no treatment truly effective to stop or reverse the progression of dementia. That’s when her daughter brought her to see me.

We discovered many subtle changes in her health that on their own wouldn’t explain dementia, but when added all together put a strain on her brain function. All we did was correct those problems — low thyroid function, mercury toxicity, inflammation, and deficiencies in vitamins B6 and D, folate, coenzyme Q10, and omega-3 fats — and improved her diet overall. I encouraged her to exercise, because exercise can help improve cognitive function and prevent dementia.

Six months later, she had the extensive memory tests repeated. Her psychologist was surprised to report that her scores got BETTER!

To put this in perspective, mental decline happens progressively, sometimes quickly, sometimes slowly, but NEVER gets better — according to our traditional medical thinking.

But just like we once thought that heart disease and artery-clogging plaques couldn’t be reversed (and now have proof that this does happen), I believe dementia can be reversed (if caught early enough) by attending to all the factors that affect brain function – diet, exercise, stress, nutritional deficiencies, toxins, hormonal imbalances, inflammation, and more.

9 Steps to Reversing Dementia

Start by looking hard for correctable causes of memory loss. They include:

  1. Pre-diabetes or metabolic syndrome
  2. Low thyroid function
  3. Depression
  4. Deficiencies in B vitamins, especially vitamin B12
  5. Omega-3 fat deficiencies
  6. Mercury or other heavy metal toxicity
  7. Vitamin D deficiency
  8. High cholesterol
  9. Unique genes that predispose you to nutritional or detoxification problems

Once you identify the underlying causes of the imbalance, here are a few things that can help your mind get a tune-up:

  • Balance your blood sugar with a whole foods, low glycemic diet
  • Exercise daily — even a 30-minute walk can help
  • Deeply relax daily with yoga, meditation, biofeedback, or just deep breathing
  • Take a multivitamin and mineral supplement
  • Take an omega-3 fat supplement
  • Take extra vitamin B6, B12, and folate
  • Take vitamin D
  • Treat thyroid or low sex hormones
  • Get rid of mercury through a medical detoxification program

This is just a start, but it can go a long way to giving your brain the chance to heal and recover if you have memory problems. Even if you aren’t suffering from cognitive decline, you should take these steps because they can help you prevent the aging of your brain and obtain lifelong health.

To your good health,

Mark Hyman, MD

References

(i) http://www.cdc.gov/nchs/fastats/lcod.htm

(ii) Tsai, M.S., Tangalos, E.G., Petersen, R.C., et al. (1994). Apolipoprotein : Risk factor for Alzheimer’s disease. American Journal of Human Genetics. 54 (4):643-649.

(iii) Godfrey, M.E., Wojcik, D.P., and C.A. Krone. (2003). Apolipoprotein E genotyping as a potential biomarker for mercury neurotoxicity. Journal of Alzheimer’s Disease. 5 (3):189-195.

(iv) Stroombergen, M.C., and R.H. Warring. (1999). Determination of glutathione S-transferase me and theta polymorphisms in neurological disease. Human and Experimental Toxicology. 18 (3):141-145.

(v) Bernardini, S., Bellincampi, L., Ballerini, S., et al. (2005). Glutathione S-transferase P1 *C allelic variant increases susceptibility for late-onset Alzheimer’s disease: Association study and relationship with Apolipoprotein E4 allele. Clinical Chemistry. 51(6):944-951.