Alzheimer's Disease & Omega-3 results

Alzheimer's disease is a progressive degenerative disease of the brain accounting for 50-70 percent of dementia. It will destroy thinking, reasoning, memory and other cognitive skills down to the core basics of simple tasks like eating. Eventually the body shuts down. The following article is a most recent publication that omega-3s can be helpful in improving memory.

Of course, chronic disease is underfunded and not being addressed efficiently. How about acute disease like H1N1 virus (if it did become a lethal killer?). An important public health report discloses we're very behind from being safe:

Gaps in Emergency Response/Trends in Response Coverage (Robert Wood Johnson Foundation Study)

Preventative medicine maybe good for the pocket book and your health too:

Reductions of acetylcholine release and nerve growth

factor expression are correlated with memory impairment induced by interleukin-1beta administrations: effects of omega-3 fatty acid EPA treatment. Release Date: December 2009

Taepavarapruk P, Song C.Department of Physiology, Faculty of Medical Science, Naresuan University, Phitsanulok, 65000, Thailand.Interleukin (IL)-1beta may play an important role in Alzheimer's disease. However, the relationships between glucocorticoids and acetylcholine (ACh), and between neurotrophins and ACh in IL-1-induced memory deficits are unknown. While ethyl-eicosapentaenoate (E-EPA) has recently been reported to reduce inflammation and improve memory, cholinergic and neurotrophic mechanisms by which E-EPA improves memory is unclear. This study evaluated 1) the correlation between ACh release and memory impairment, 2) the effect of glucocorticoids on ACh release; 3) the relationship between nerve growth factor (NGF) and inflammation, and 4) the effects of E-EPA treatment on IL-1beta-induced changes. Intracerebroventricular IL-1beta administrations produced a significant reduction in hippocampal ACh release in rats fed control diet, which was partially attenuated by RU 486 and completely blocked by IL-1RA. In 8-arm radial maze, significantly less ACh release was correlated with the memory deficits after IL-1beta administrations. mRNA expression of hippocampal NGF was lower, while IL-1beta was higher when compared to controls. E-EPA treatment significantly improved the memory, which was correlated with normalizing ACh release, and expressions of NGF and IL-1beta. The present study revealed important mechanisms by which IL-1beta impairs, while E-EPA improves memory through IL-1-glucocorticoid-ACh release and IL-1-NGF-ACh release pathways.