curcumin

High iron, copper levels block neuron repair

June, 2011

New findings help explain why too much copper and iron are bad for your brain, and why curry is good for it.

A new study finds out why curcumin might help protect against dementia, and links two factors associated with Alzheimer’s and Parkinson’s diseases: DNA damage by reactive oxygen species (ROS), and excessive levels of copper and iron in parts of the brain. It turns out that high levels of copper or iron help generate large numbers of ROS and interfere with DNA repair.

While small amounts of iron and copper are vital, these are normally bound by proteins. However, when there’s too much, it can overwhelm the proteins and the result is "free" iron or copper ions circulating in the blood, able to initiate chemical reactions that produce reactive oxygen species. Moreover, the free copper and iron also interferes with the activity of two enzymes that repair DNA, NEIL1 and NEIL2.

However, the curry spice curcumin binds to iron and copper and was extremely effective in protecting the NEIL enzymes from the metals.

Reference: 

Hegde, M.L., Hegde, P.M. , Rao, K.S.J. & Mitra, S. 2011. Oxidative Genome Damage and Its Repair in Neurodegenerative Diseases: Function of Transition Metals as a Double-Edged Sword. Journal of Alzheimer's Disease , 25 (1), 183-198.

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Compound derived from curry spice helps in stroke and TBI

January, 2011

Two new animal studies offer hope for a drug treatment for traumatic brain injury and stroke.

Following indications that the curry spice curcumin (the active ingredient in turmeric) may help protect brain cells from damage, two new studies have been testing a compound called CNB-001, derived from curcumin.

The first (rabbit) study found that CNB-001 is at least as effective as the only existing drug used to treat stroke (TPA), without the unwanted side-effect of reducing clotting in the blood vessels of the brain.

The second study found that CNB-001 dramatically reversed the behavioral deficits in both locomotion and memory in brain-injured rats. As with stroke, CNB-001 was again found to maintain the critical signaling pathways required for nerve cell survival, as well as the connections between nerve cells that are lost with the injury.

At present, there is no treatment for TBI, and only one FDA-approved drug for ischemic stroke

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