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This post was written during early stages of trying to understand a complex scientific problem, and we didn't get everything right. The original author no longer endorses the content of this post. It is being left online for historical reasons, but read at your own risk.
“Potential therapeutic effects of curcumin, the anti-inflammatory agent, against neurodegenerative, cardiovascular, pulmonary, metabolic, autoimmune, and neoplastic diseases,” Aggrawal and Harikumar, Int J Biochem Cell Biol (2009)
Although safe in most cases, ancient treatments are ignored because neither their active component nor their molecular targets are well defined. This is not the case, however, with curcumin, a yellow-pigment substance and component of turmeric (Curcuma longa), which was identified more than a century ago. For centuries it has been known that turmeric exhibits anti-inflammatory activity, but extensive research performed within the past two decades has shown that the this activity of turmeric is due to curcumin, a diferuloylmethane. This agent has been shown to regulate numerous transcription factors, cytokines, protein kinases, adhesion molecules, redox status and enzymes that have been linked to inflammation. The process of inflammation has been shown to play a major role in most chronic illnesses, including neurodegenerative, cardiovascular, pulmonary, metabolic, autoimmune and neoplastic diseases. In the current review, we provide evidence for the potential role of curcumin in the prevention and treatment of various pro-inflammatory chronic diseases. These features, combined with the pharmacological safety and negligible cost, render curcumin an attractive agent to explore further.
“Curcumin inhibits dose-dependently and time-dependently neuroglial cell proliferation and growth,” Ambegaokar et al., Neuroendocrinology Letters (2003)
It is generally recognized that the inflammation with increased microglia and astrocytic cliosis that surrounds amyloid plaques, the neurofibrillary debris and other pathologic lesions characteristic of neurodegenerative diseases may contribute to their etiology and progressive worsening . The beneficial effects of curcumin in prevention/treatment of these diseases may be due to its anti-inflammatory actions through inhibition of microglia and astrocytic proliferation.
In our present data, curcumin appears to act on neuroglia cells by promoting oligodendritic differentiation, improving myelinogenesis, and reducing astrocytic proliferation.
The present data suggest that dose and time factors should be considered in further CUR research. For neuroglial cell culture and other in vitro experiments, concentrations between 15uM and 30uM are more effective for short trials (<24 hours), while concentrations between 5uM and 15uM are better suited for longer studies (4 to 6 days). It is foreseeable that the 4um concentration would show inhibition of proliferation if treated for al longer period (8 to 10 days.) … It is possible that very small doses (≤1uM) may be as effective as higher doses if used for a longer period.
“Targeting multiple neurodegenerative diseases etiologies with multimodal-acting green tea catechins,” Mandel et al., J Nutr. (2008)
Green tea is currently considered a source of dietary constituents endowed with biological and pharmacological activities relevant to human health. Human epidemiological and new animal data suggest that the pharmacological benefits of tea drinking may help to protect the brain as we age. Indeed, tea consumption is inversely correlated with the incidence of dementia and Alzheimer’s and Parkinson’s diseases. In particular, its main catechin polyphenol constituent (-)-epigallocatechin-3-gallate has been shown to exert neuroprotective/neurorescue activities in a wide array of cellular and animal models of neurological disorders. The intense efforts dedicated in recent years to shed light on the molecular mechanisms participating in the brain protective action of green tea indicate that in addition to the known antioxidant activity of catechins, the modulation of signal transduction pathways, cell survival/death genes, and mitochondrial function all contribute significantly to the induction of neuron viability. Because of the multietiological character of neurodegenerative disease pathology, these natural compounds are receiving significant attention as therapeutic cytoprotective agents that simultaneously manipulate multiple desired targets in the central nervous system. This article elaborates on the multimodal activities of green tea polyphenols with emphasis on their recently described neurorescue/neuroregenerative and mitochondrial stabilization actions.
“Understanding the broad-spectrum neuroprotective action profile of green tea polyphenols in aging and neurodegenerative diseases,” Mandel et al., J. Alzheimers Dis. (2011)
Human epidemiological and new animal data suggest that green and black tea drinking (enriched in a class of flavonoids named catechins) may help protecting the aging brain and reduce the incidence of dementia, AD, and PD. Mechanistic studies on the neuroprotective/
neuroregenerative effects of green tea catechins revealed that they act not only as antioxidants metal chelators, but also as modulators of intracellular neuronal signaling and metabolism, cell survival/death genes, and mitochondrial function. Thus, these dietary compounds are receiving significant attention as therapeutic multifunctional cytoprotective agents that simultaneously manipulate various brain targets. The scope of this review is to assess and put into perspective salient features of the beneficial brain action of natural, non-toxic green tea catechins in aging-impaired cognition and neurodegenerative diseases and to discuss a scenario concerning their potential, in drug combination, to target distinct pathologies, in the quest for a disease modifying therapy.
“Green tea catechins as brain-permeable, natural iron chelators-antioxidants for the treatment of neurodegenerative disorders,” Mandel et al., Mol Nutr Food Res (2006)
Neurodegeneration in Parkinson’s, Alzheimer’s, or other neurodegenerative diseases appears to be multifactorial, where a complex set of toxic reactions, including oxidative stress (OS), inflammation, reduced expression of trophic factors, and accumulation of protein aggregates, lead to the demise of neurons. One of the prominent pathological features is the abnormal accumulation of iron on top of the dying neurons and in the surrounding microglia. The capacity of free iron to enhance and promote the generation of toxic reactive oxygen radicals has been discussed numerous times. The observations that iron induces aggregation of inert alpha-synuclein and beta-amyloid peptides to toxic aggregates have reinforced the critical role of iron in OS-induced pathogenesis of neurodegeneration, supporting the notion that a combination of iron chelation and antioxidant therapy may be one significant approach for neuroprotection. Tea flavonoids (catechins) have been reported to possess divalent metal chelating, antioxidant, and anti-inflammatory activities, to penetrate the brain barrier and to protect neuronal death in a wide array of cellular and animal models of neurological diseases. This review aims to shed light on the multipharmacological neuroprotective activities of green tea catechins with special emphasis on their brain-permeable, nontoxic, transitional metal (iron and copper)-chelatable/radical scavenger properties.
Society For Neuroscience (2007, November 6). Diet Of Walnuts, Blueberries Improve Cognition; May Help Maintain Brain Function.
ScienceDaily. Retrieved December 28, 2011, from http://www.sciencedaily.com /releases/2007/11/
In other recent studies, Ron Mervis, PhD, of the Center for Aging and Brain Repair at the University of South Florida College of Medicine in Tampa, Fla., who collaborated with Joseph and Shukitt-Hale, has discovered that supplementing the diet of old rats with blueberries for a relatively short period (8 weeks), resulted in maintenance and rejuvenation of brain circuitry. These results, using a small amount of blueberry extract, two percent, to supplement a standard rat diet, are the first to show that a dietary intervention, specifically blueberries, can not only protect against the loss of dendritic branching and dendritic spines (e.g., synapses) seen in aged animals, but can result in neuroplastic enhancement of brain circuitry such that it looks like a much younger brain.
Mervis explains that age-related oxidation and inflammation in the brain can damage neurons. He notes that blueberries also contain various chemical compounds-flavonoids-which have strong antioxidant and anti-inflammatory activities.
“These benefits, along with other indirect mechanisms, may help to minimize, or reverse, the age-related breakdown of communication between neurons,” says Mervis, “and optimize brain function in the old rat.” A two percent blueberry extract is equivalent to a human having about half a cup of blueberries added to their daily diet.
Vitamin D (from Wikipedia):
- Fatty fish species, such as:
- Catfish, 85 g (3 oz) provides 425 IU (5 IU/g)
- Salmon, cooked, 100 g (3.5 oz) provides 360 IU (3.6 IU/g)
- Mackerel, cooked, 100 g (3.5 oz), 345 IU (3.45 IU/g)
- Sardines, canned in oil, drained, 50 g (1.75 oz), 250 IU (5 IU/g)
- Tuna, canned in oil, 100 g (3.5 oz), 235 IU (2.35 IU/g)
- Eel, cooked, 100 g (3.5 oz), 200 IU (2.00 IU/g)
- A whole egg provides 20 IU if egg weighs 60 g (3 IU/g)
- Beef liver, cooked, 100 g (3.5 oz), provides 15 IU (0.15 IU/g)
- Fish liver oils, such as cod liver oil, 1 Tbs. (15 ml) provides 1360 IU (90.6 IU/ml)
- UV-irradiated mushrooms and yeast are the only known vegan significant sources of vitamin D from food sources. Exposure of portabella mushrooms to UV provides an increase of vitamin D content in an 100-g portion (grilled) from about 14 IU (0.14 IU/g non-exposed) to about 500 IU (5 IU/g exposed to UV light).
Vitamin E (from Wikipedia):
Some foods with vitamin E content mg/(100 g)
150 Wheat germ oil
34 Safflower oil
15 Palm oil 
1.5 Kiwifruit (green)
- ^ Dowd, P; Zheng, Z. B. (1995). “On the mechanism of the anticlotting action of vitamin E quinone”. Proc Natl Acad Sci U S A. 92 (18): 8171–8175. doi:10.1073/pnas.92.18.8171. PMC 41118. PMID 7667263.
- ^ Brigelius-Flohé; Davies, KJ (2007). “Is vitamin E an antioxidant, a regulator of signal transduction and gene expression, or a ‘junk’ food? Comments on the two accompanying papers: “Molecular mechanism of alpha-tocopherol action” by A. Azzi and “Vitamin E, antioxidant and nothing more” by M. Traber and J. Atkinson”. Free radical biology & medicine 43 (1): 2–3. doi:10.1016/j.freeradbiomed.
2007.05.016. PMID 17561087.
- ^ Atkinson; Epand, RF; Epand, RM (2008). “Tocopherols and tocotrienols in membranes: a critical review”. Free radical biology & medicine 44 (5): 739–64. doi:10.1016/j.freeradbiomed.
2007.11.010. PMID 18160049