October 19, 2010

Luteolin may help prevent memory loss

Rodney Johnson and his associates at the University of Illinois report in the October, 2010 issue of the Journal of Nutrition that the flavonoid luteolin helped reduce inflammation in the brains of aged mice, which restored memory to levels observed in younger animals.

Luteolin is found in carrots, rosemary, celery and other foods. The study's findings could have applications for treating memory loss in older humans.

The current research, funded by the National Institutes of Health, examined luteolin's effect in immune cells in the brain known as microglial cells, which produce inflammatory signaling molecules in response to infection. “We found previously that during normal aging, microglial cells become dysregulated and begin producing excessive levels of inflammatory cytokines,” explained Dr Johnson, who is the director of the University of Illinois Division of Nutritional Sciences. “We think this contributes to cognitive aging and is a predisposing factor for the development of neurodegenerative diseases.”

When Dr Johnson and his colleagues exposed microglial cells to a bacterial toxin, they produced inflammatory cytokines capable of destroying brain cells known as neurons. While pretreatment of neurons with luteolin showed no benefit, exposure of microglia to this compound prevented neuron death. “This demonstrated that luteolin isn’t protecting the neurons directly,” Dr Johnson stated. “It’s doing it by affecting the microglial cells. The neurons survived because the luteolin inhibited the production of neurotoxic inflammatory mediators.”

In an experiment with mice, adult and aged animals were fed a control diet or a luteolin-enhanced diet for four weeks. Assessment of spatial memory found increased learning and recall in older mice supplemented with luteolin compared to aged controls. In addition, inflammatory markers in the brain's hippocampus, a region involved in spatial awareness and memory, were decreased. “When we provided the old mice luteolin in the diet it reduced inflammation in the brain and at the same time restored working memory to what was seen in young cohorts,” Dr Johnson stated. “We believe dietary luteolin accesses the brain and inhibits or reduces activation of microglial cells and the inflammatory cytokines they produce. This anti-inflammatory effect is likely the mechanism which allows their working memory to be restored to what it was at an earlier age.”

The study is the first to indicate that luteolin increases cognitive function by acting on the microglial cells. “These data suggest that consuming a healthy diet has the potential to reduce age-associated inflammation in the brain, which can result in better cognitive health,” Dr Johnson concluded.

Chronic inflammation

Aging results in an increase of inflammatory cytokines (destructive cell-signaling chemicals) that contribute to the progression of many degenerative diseases (Van der Meide et al. 1996; Licinio et al. 1999). Rheumatoid arthritis is a classic autoimmune disorder in which excess levels of cytokines such as tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6), interleukin 1b [IL-1(b)], and/or interleukin-8 (IL-8) are known to cause or contribute to the inflammatory syndrome (Deon et al. 2001).

Chronic inflammation is also involved in diseases as diverse as atherosclerosis, cancer, heart valve dysfunction, obesity, diabetes, congestive heart failure, digestive system diseases, and Alzheimer's disease (Brouqui et al. 1994; Devaux et al. 1997; De Keyser et al. 1998). In aged people with multiple degenerative diseases, the inflammatory marker, C-reactive protein, is often sharply elevated, indicating the presence of an underlying inflammatory disorder (Invitti 2002; Lee et al. 2002; Santoro et al. 2002; Sitzer et al. 2002). When a cytokine blood profile is conducted on people in a weakened condition, an excess level of one or more of the inflammatory cytokines, e.g., TNF-a, IL-6, IL-1(b), or IL-8, is usually found (Santoro et al. 2002).

In addition to toxic cytokines, there are other inflammatory pathways that can be mediated via diet modification. A common problem involves overproduction of pro - inflammatory hormone-like "messengers" (such as prostaglandin E2) and underproduction of anti-inflammatory "messengers" (such as prostaglandin E1 and E3).

The good news is that omega-3 fatty acids found in fish oil help to suppress the formation of undesirable prostaglandin E2 and promote synthesis of beneficial prostaglandin E3 (Kelley et al. 1985; Watanabe et al. 2000).

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