Artificial Butter Flavoring Ingredient Linked to Key Alzheimer’s Disease Process

A new study raises concern about chronic exposure of workers in industry to a food flavoring ingredient used to produce the distinctive buttery flavor and aroma of microwave popcorn, margarines, snack foods, candy, baked goods, pet foods and other products. It found evidence that the ingredient, diacetyl (DA), intensifies the damaging effects of an abnormal brain protein linked to Alzheimer’s disease. The study appears in ACS’ journal Chemical Research in Toxicology.

Alzheimer’s villain cures multiple sclerosis in mice

A notorious biochemical villain has just revealed its heroic side. Beta-amyloid, a misfolded protein fragment blamed for killing brain cells in Alzheimer’s disease, has reversed the symptoms of mice suffering from the rodent equivalent of multiple sclerosis (MS).

MS occurs when the immune system mistakenly attacks the fatty myelin sheaths around nerve fibres that serve as electrical insulation. Without this insulation, nervous impulses falter, leading to physical and cognitive problems. Myelin increases the speed at which electrical impulses travel around the body.

As it is destroyed, nerve communication falters, leading to physical and cognitive problems. Lawrence Steinman of Stanford University in California had expected amyloid-beta to exacerbate this damage, given that it is toxic to neurons and builds up where myelin sheaths are being destroyed.

How the Brain and Nerve Cells Change During Alzheimer’s Disease

One of the hallmarks of Alzheimer’s disease is the accumulation of amyloid plaques between nerve cells (neurons) in the brain. Beta amyloid is a fragment of a protein snipped from another protein called amyloid precursor protein (APP). In a healthy brain, these protein fragments would break down and be eliminated. In Alzheimer’s disease, the fragments accumulate to form hard, insoluble plaques.

Neurofibrillary tangles are insoluble twisted fibers found inside the brain’s nerve cells. They primarily consist of a protein called tau, which forms part of a structure called a microtubule. The microtubule helps transport nutrients and other important substances from one part of the nerve cell to another. Axons are long threadlike extensions that conduct nerve impulses away from the nerve cell; dendrites are short branched threadlike extensions that conduct nerve impulses towards the nerve cell body. In Alzheimer’s disease the tau protein is abnormal and the microtubule structures collapse.

As Alzheimer’s disease spreads through the cerebral cortex (the outer layer of the brain), judgment worsens, emotional outbursts may occur and language is impaired. Memory worsens and may become almost non-existent. On average, those with Alzheimer’s live for 8 to 10 years after diagnosis, but this terminal disease can last for as long as 20 years.

The Aging Brain Is More Malleable Than Previously Believed 

There is growing evidence that, beyond what was previously believed, the adult human brain is remarkably malleable and capable of new feats — even in the last decades of life.

In fact, new experiences can trigger major physical changes in the brain within just a few days, and certain conditions can accelerate this physical, chemical and functional remodeling of the brain.

"We used to think that the brain was completely formed by development and its basic structure didn’t change much in adults, but as research went on we discovered that wasn’t true, at least in the cerebral cortex," explains Randy Bruno, a member of the Kavli Institute for Brain Science at Columbia University. "We now know that an underlying portion of the brain called the thalamus, which feeds the cortex information from our senses, is also remarkably plastic."

Brain Expression

Researchers map the expression patterns of 1,000 genes in the human brain. 

The paper

H. Zeng et al., “Large-scale cellular-resolution gene profiling in human neocortex reveals species-specific molecular signatures,” Cell, 149:48-96, 2012.

The finding

Whole-genome sequencing has given researchers a good sense of which genes are shared between, for example, humans and mice. But little is known about how the expression patterns of these genes differ. Hongkui Zeng of the Allen Institute for Brain Science in Seattle, Washington, and colleagues took slices of human brains collected from postmortem biopsies and tested the expression of 1,000 key neuronal genes. They found that about 21 percent of the gene-expression profiles differed between the two species.

The sliver

Researchers took thin slices from regions of the brain involved in processing visual and sensory information and scanned them for the in situ expression of 1,000 genes that act as markers of cell type or are involved in disease, evolution, or cortical function. They compared gene expression of three areas of the cortex across 46 donors with corresponding mouse-brain slices, which had been analyzed previously at the Allen Institute.

The difference

The differences between humans and mice “often manifested in a cell type-specific way,” said Zeng, or involved in between-cell communications. “The disease genes are all very well conserved,” which bodes well for researchers using mice as models of disease, she says.

The impact

“The mouse model is used extensively in neuroscience research, and it’s assumed to be a surrogate for the human,” says Daniel Geschwind, a neurogeneticist at the University of California, Los Angeles. Knowing the specific differences “gives you a sense that many things are conserved, but also provides some guidance as to the ones that aren’t.”

dailymedical:

Goodbye, IQ Tests: Brain Imaging Can Reveal Intelligence Levels

Research from Washington University in St. Louis has identified variations in brain scans that they believe identify portions of the brain that are responsible for intelligence.

As suspected (and as explained by cartoons) brain size does play a small role; they said that brain size accounts for 6.7 percent of variance in intelligence. Recent research has placed the brain’s prefrontal cortex, a region just behind the forehead, as providing for 5 percent of the variation in intelligence between people.

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Sick from Stress? Blame Your Mom… And Epigenetics

If you’re sick from stress, a new research report appearing in the August 2012 issue of The FASEB Journal suggests that what your mother ate — or didn’t eat — may be part of the cause. The report shows that choline intake that is higher than what is generally recommended during pregnancy may improve how a child responds to stress. These improvements are the result of epigenetic changes that ultimately lead to lower cortisol levels. Epigenetic changes affect how a gene functions, even if the gene itself is not changed. Lowering cortisol is important as high levels of cortisol are linked to a wide range of problems ranging from mental health to metabolic and cardiovascular disorders.

The Unbalanced Sloth

Most creatures need a good sense of balance — especially tree-dwellers that swing among high branches. In mammals, the ability largely comes from three loop-shaped structures in the inner ear called semicircular canals; in most species, the size, shape, and arrangement of those loops (inset) is extremely consistent from one individual to another. But in three-toed sloths (such as Bradypus variegatus, the brown-throated three-toed sloth, pictured), many proportions of the semicircular canals are surprisingly variable from one sloth to another.

The overall variability is at least twice that seen in other species of mammals the team analyzed, researchers report online today in the Proceedings of the Royal Society B. That high degree of variation stems from the sloths’ languid lifestyle, the researchers suggest.

Sloths, which move extremely slowly when they move at all, don’t require the sense of balance that a swift, agile creature such as a primate needs. The finding supports one of Charles Darwin’s notions about evolution: If an organ isn’t crucial, variations in its structure or performance aren’t lost over time, keeping the potpourri in the population.