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Discovery Helps Pin Alzheimer’s Risk on Free Radicals
2/12/2007
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Findings in fruit flies support wisdom of consuming antioxidant-rich tea, cocoa, spices, herbs, vegetables, and fruits

by Craig Weatherby


The mystery of what causes Alzheimer’s disease and related forms of dementia has resisted efforts to find its solution.


Alzheimer’s is characterized by buildup of cell-killing plaques and tangles in the brain, but it’s been unclear whether these phenomena cause the disease or are just symptom-exacerbating manifestations of it.


It’s also been unclear whether inflammation-inducing free radicals in people’s diets and internal environments cause or simply promote formation of plaques and tangles.


In other words, we face major chicken-or-egg challenges to untangling the underlying causes of Alzheimer’s.


Now, intriguing results from fruit fly experiments may have finally collared the brain-damaging criminal. If they hold up over time, these tests will be seen as the first to prove that “oxidative stress”and a deficiency of sufficient antoixdant defensesdoes indeed cause Alzheimer’s disease.


First, let’s take a look at the issue of free radicals and inflammation in Alzheimer’s disease and related form of dementia.


Free radicals and dementia: a tangled tale

Oxidative stress is the gene-switching, inflammation-inducing, cell-damaging chain reaction initiated by the various kinds of unstable oxygen molecules collectively called free radicals.


Free radicals flow primarily from our own metabolic processes, and are normally neutralized by our bodies’ “antioxidant network” of enzymes.


The body's ability to make enough of some key antioxidantsincluding glutathione peroxidase and thioredoxin reductasedepends on adequate supplies of dietary selenium.


This oft-overlooked mineral is abundant in only a few foodsnotably, brazil nuts, garlic, and ocean fishnd it is lacking in some key regional soils, so foods grown in them will be selenium-poor (e.g., much of the upper Midwest and China).


Free radicals also occur in polluted air and water, and are generated by pro-inflammatory diets high in sugars and starches or the omega-6 fatty acids that dominate common vegetable oils and hydrogenated oils.


And free radicals have a freer reign to induce inflammation, cell damage, and creation of more free radicals when people’s diets lack enough colorful, antioxidant-rich plant foods or adequate amounts of the anti-inflammatory omega-3s in leafy greens and seafood.


An ever-growing body of evidence indicates that diets rich in antioxidants from colorful vegetables and fruits yield significantly reduced risks of Alzheimer’s and age-related cognitive declines and dementias.


This includes many cell, animal and epidemiological studies on curcumin: the potent polyphenol-type antioxidant pigment that makes turmeric bright yellow. For more on this, search our newsletter archive.


And the positive results of several epidemiological studies suggest that fish and omega-3-rich fish oils also help prevent dementia. Omega-3s reduce free-radical-generating inflammation and stabilize brain-cell membranes, while fish flesh supplies lots of selenium.


As a UCLA brain researcher who authored a recent evidence review put it, “We have shown that the consumption of a diet rich in saturated fat decreases learning and memory and increases metabolic distress. Conversely, diets supplemented either with omega-3 fatty acids, vitamin E or the curry spice curcumin benefit cognitive function” (Pinilla FG 2006).


The results of a new study from Harvard Medical School and Brigham and Women’s Hospital in Boston offer encouragement that diet may offer a way to prevent or ameliorate the brain damage that yields dementia (Dias-Santagata D et al 2007).


Fruit fly study accentuates value of antioxidants

The Boston group used a clever study design to test the effects and role of polyphenol-type antioxidants: the kind found in tea, cocoa, herbs, spices, fruits, and vegetables.


First, they manipulated the genes responsible for the production of two key internal antioxidant enzymessuperoxide dismutase (SOD) and thioredoxin reductase (Trxr)to reduce their production in the flies.


Thanks to previous studies, the scientists knew that hindering production of SOD and Trxr would allow the formation of rogue “tau” proteins that form the protein tangles characteristic of Alzheimer’s patients’ brains (Khurana V et al 2006; Ferrer I et al 2005).


Then they fed vitamin Ea potent, polyphenol-type anti-oxidantto the mutant flies.


As expected, the artificially induced reduction in production of two key antioxidant enzymes in the flies, led to expression of the gene that promotes production of tau proteins, and caused a buildup of tau-protein tangles in their brains.


(Non-mutated control flies did not express the gene for production of tau protein and did not show any signs of brain degeneration or Alzheimer’s-type protein tangles and plaques.)


And as hoped, administration of vitamin E reversed this damaging effect.


Together, these results provide strong evidence that oxidative stress plays an important role in Alzheimer’s and similar dementias that involve the tau protein.


Logically, this suggests that antioxidant-rich diets can protect and enhance brain health.


As the Harvard team put it, “Our results suggest that increased levels of oxidative stress play an active role in enhancing tau-mediated neurodegeneration [brain-cell damage]… underscoring the therapeutic potential of targeting antioxidant pathways and cell cycle mechanisms for the [prevention] of AD [Alzheimer’s disease]” (Dias-Santagata D et al 2007).


It goes without saying that we need to confirm that the same mechanisms work in humans, but the available evidence indicates that they do.



Sources

  • Dias-Santagata D, Fulga TA, Duttaroy A, Feany MB. Oxidative stress mediates tau-induced neurodegeneration in Drosophila. J Clin Invest. 2007 Jan 2;117(1):236-245. Epub 2006 Dec 14.
  • Khurana V, Lu Y, Steinhilb ML, Oldham S, Shulman JM, Feany MB. TOR-mediated cell-cycle activation causes neurodegeneration in a Drosophila tauopathy model. Curr Biol. 2006 Feb 7;16(3):230-41.
  • Ferrer I, Gomez-Isla T, Puig B, Freixes M, Ribe E, Dalfo E, Avila J. Current advances on different kinases involved in tau phosphorylation, and implications in Alzheimer's disease and tauopathies. Curr Alzheimer Res. 2005 Jan;2(1):3-18. Review.
  • Pinilla FG. The impact of diet and exercise on brain plasticity and disease. Nutr Health. 2006;18(3):277-84. Review.

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