Takayuki Tamura and colleagues note that wine connoisseurs established the rule of thumb because of the flavor clash between red wine and fish. They point out, however, that there are exceptions to the rule, with some red wines actually going well with seafood. Until now, nobody could consistently predict which wines might trigger a fishy aftertaste because of the lack of knowledge about its cause.

The researchers asked wine tasters to sample 38 red and 26 white wines while dining on scallops. Some of the wines contained small amounts of iron, which varied by country of origin, variety, and vintage. They found that wines with higher amounts of iron had a more intensely fishy aftertaste. This fishy taste diminished when they added a substance that binds up iron. The findings indicate that iron is the key factor in the fishy aftertaste of wine-seafood pairings, the researchers say, suggesting that low-iron red wines might be a good match with seafood.

Journal reference:

Tamura et al. Iron Is an Essential Cause of Fishy Aftertaste Formation in Wine and Seafood Pairing. Journal of Agricultural and Food Chemistry, 2009; 57 (18): 8550 DOI: 10.1021/jf901656k

The retina is a light-sensitive tissue that lines the inner surface of the eye. The optics of the eye form an image of the visual world on the retina, similar to film in a camera.  When light strikes the retina, a cascade of chemical and electrical events is initiated that ultimately trigger nerve impulses. These are then sent to various ‘visual centers’ of the brain through the fibers of the optic nerve.

In development, the retina and the optic nerve begin as outgrowths of the developing brain (so the retina is considered part of the central nervous system – CNS).  It’s actually the only part of the CNS that can be imaged non-invasively in the living organism.

The retina itself is a complex structure with several layers of neurons interconnected by synapses. The photoreceptor cells are the only neurons that are directly sensitive to light.  These are of two types: the rods and cones. Rods work mainly in dim light and provide black-and-white vision, while the cones support daytime vision and the perception of color. A third, less common type of photoreceptor is the photosensitive ganglion cell, which is important for reflexive responses to bright daylight.

A recent study was conducted exploring the restoration of defective retinas.  In this study, an array of electrodes implanted on the back of the eye, forming an artificial retina, was found to restore partial vision to totally blind people.  In a recent study of 15 blind participants who had the implant for three months, 10 of the patients tested were able to identify the direction of moving objects.

These findings were presented at the annual meeting of the Society for Neuroscience, Neuroscience 2009.

“These results give new hope to the many people with degenerative retinal diseases,” said Jessy Dorn, PhD, of Second Sight Medical Products, Inc., lead author of the study.   Over two million Americans suffer from diseases of the eye such as retinitis pigmentosa (a type of progressive retinal dystrophy) and age-related macular degeneration.  These patients slowly lose their vision as the nerve cells that detect light are destroyed, due to either age or illness. There is no known cure.

In the research presented, they worked around the damaged cells. The participants were given glasses, with a small video camera attached, as well as a small computer hooked to a belt.  After receiving video images from the camera, the computer processed them and transmitted the data to the implanted electrodes on the retina.  The participants watched a monitor with a white bar sweeping across a black screen, and the electrodes that corresponded with the moving bar stimulated cells in the eye, which created spots of light in their fields of vision.

“We found that most of the study participants were better able to determine the direction of the bar when using the prosthesis system than without it, or with a scrambled video input,” Dorn said. “In other words, this new system gave most blind people the ability to identify an object’s direction of motion — something they could not do without it.” This technology is now being tested in an international clinical trial.  So far, 32 blind people have received the implant.

Although this is far from a perfect system, it is encouraging that the link between technology and biology is now able to partially restore one of our basic senses.

Research was supported by the National Eye Institute.

Unfortunately, the cause and progression of Alzheimer’s disease are not well understood. Research indicates that the disease is associated with plaques and tangles in the brain.  The current treatments offer a small symptomatic benefit, but no treatments exist to delay or halt the progression of the disease.  A number of non-invasive, life-style habits have been suggested for the prevention of Alzheimer’s disease, but there is a lack of adequate evidence for a link between these recommendations and reduced degeneration. Mental stimulation, exercise, and a balanced diet are suggested, as both a possible prevention and a sensible way of managing the disease.

The main hypothesis regarding Alzheimer’s disease suggests that the fundamental cause is the deposition of amyloid beta (Aβ) in the brain. Support comes from the location of the gene for the amyloid beta precursor protein (APP) on chromosome 21.  People with trisomy 21 (Down Syndrome), who have an extra gene copy, almost universally exhibit Alzheimer’s disease by age 40. APOE4, the major genetic risk factor for Alzheimer’s, leads to excess amyloid buildup in the brain before symptoms arise. In this way, Aβ deposition precedes clinical Alzheimer’s disease. More evidence comes from the finding that transgenic mice that express a mutated form of the human APP gene develop fibrillar amyloid plaques and Alzheimer’s-like brain pathology with spatial learning deficits.

Recently (early 2009-ish), it was found that oligomeric Aβ has a toxic effect on brain physiology by binding to a specific receptor on neurons.  This receptor is the prion protein, which has been linked to mad cow disease and the related human condition, Creutzfeldt-Jakob disease.  This provides a link in the underlying mechanism of these neurodegenerative disorders with that of Alzheimer’s disease.

A discovery by scientists from the Mayo Clinic in Jacksonville, FL, could lead to a new treatment for Alzheimer’s Disease that actually eliminates amyloid plaques from patients’ brains.

Published online in The FASEB Journal, the discovery is based on the unexpected finding that when the immune cells of the brain (microglia) are activated by the interleukin-6 protein (IL-6), they actually remove plaques instead of causing them or making them worse. The research was conducted in a model of Alzheimer’s disease established in mice.

“Our study highlights the notion that manipulating the brain’s immune response could be translated into clinically tolerated regimens for the treatment of neurodegenerative diseases,” said Pritam Das, co-author of the study, from the Mayo Clinic in Jacksonville, FL.

Das and colleagues found this unexpected phenomenon when they set out to prove that the activation of microgila triggers an inflammatory response, eventually making the disease worse. Their hypothesis was that microglia would try to eliminate the plaques, but wouldn’t be able to do so, and in the process cause excessive inflammation. Surprisingly, when microglia were activated by IL-6, they cleared the plaques from the brains.

IL-6 was over-expressed in the brains of newborn mice that had yet to develop any amyloid plaques, as well as in mice with pre-existing plaques. Using a technique called somatic brain transgenesis, they analyzed the effect of IL-6 on brain neuro-inflammation and plaque deposition. In both groups of mice, the presence of IL-6 lead to the clearance of amyloid plaques from the brain. The researchers then set out to determine exactly how IL-6 worked to clear the plaques and found that the inflammation induced by IL-6 directed the microglia to express proteins that removed the plaques. This finding suggests that manipulating the brain’s own immune cells with inflammatory mediators could lead to new therapies for the treatment of neurodegenerative diseases, particularly Alzheimer’s disease.

Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal, had this to say.  “This model is as close to human pathology as animal models get. These results give us an exciting lead to newer, more effective treatments of Alzheimer’s disease.  This study demonstrates that investment in experimental biology is the best way to approach the challenge posed by an aging population to the cost of health care.”

Although this study does not address the negative effects of stimulating inflammation in the brain, it provides some potential for a treatment.  A separate experimental vaccine was previously found to clear the amyloid plaques in early human trials, but it did not have any significant effect on dementia.  It will be interesting to see where this research leads, as any therapeutic discoveries offer hope in the face of this devastating disease.

Reference:

Paramita Chakrabarty, Karen Jansen-West, Amanda Beccard, Carolina Ceballos-Diaz, Yona Levites, Christophe Verbeeck, Abba C. Zubair, Dennis Dickson, Todd E. Golde, and Pritam Das. Massive gliosis induced by interleukin-6 suppresses A  deposition in vivo: evidence against inflammation as a driving force for amyloid deposition. The FASEB Journal, 2009; DOI: 10.1096/fj.09-141754 PMID: 19825975