Iron is a popular topic in health news. Doctors prescribe it for medical reasons, and it's available over the counter as a dietary supplement. And while it's known that too little iron can result in cognitive problems, it's also known that too much promotes neurodegenerative diseases.

Now, researchers at UCLA have found that in addition to causing cognitive problems, a lack of iron early in life can affect the brain's physical structure as well.

New research at Oregon State University provides evidence for the first time that disruption of circadian rhythms - the biological "clocks" found in many animals - can clearly cause accelerated neurodegeneration, loss of motor function and premature death.

The study was published in Neurobiology of Disease and done by researchers at OSU and Oregon Health and Science University. Prior to this, it wasn't clear which came first - whether the disruption of biological clock mechanisms was the cause or the result of neurodegeneration.

"In these experiments, we showed through both environmental and genetic approaches that disrupting the biological clock accelerated these health problems," said Kuntol Rakshit, an OSU graduate fellow.

With a lack of effective treatments for Alzheimer's, most of us would think long and hard about whether we wanted to know years in advance if we were genetically predisposed to develop the disease. For researchers, however, such knowledge is a window into Alzheimer's disease's evolution.

Understanding the biological changes that occur during the clinically "silent" stage - the years before symptoms appear - provides clues about the causes of the disease and may offer potential targets for drugs that will stop it from progressing.

Wearing a nicotine patch may help improve memory loss in older adults with mild cognitive impairment, according to a study published in Neurology, the medical journal of the American Academy of Neurology.

The study looked at individuals with mild cognitive impairment (MCI), the stage between normal aging and dementia when others begin to notice that an individual is developing mild memory or thinking problems. Many older adults with MCI go on to develop Alzheimer's disease.

Two related studies from Northwestern University offer new strategies for tackling the challenges of preventing and treating diseases of protein folding, such as Alzheimer's, Parkinson's and Huntington's diseases, amyotrophic lateral sclerosis (ALS), cancer, cystic fibrosis and type 2 diabetes.

To do its job properly within the cell, a protein first must fold itself into the proper shape. If it doesn't, trouble can result. More than 300 diseases have at their root proteins that misfold, aggregate and eventually cause cellular dysfunction and death.

The loss of manganese could mean that calcium does not stick to bones and could cause osteoporosis. This is the new theory put forward by researchers at the University of Castilla-La Mancha (UCLM) in Spain after studying deer antlers. The hypothesis published this month in the Frontiers of Bioscience journal still needs to be confirmed by the scientific community.

New research has found that elderly people with higher levels of several vitamins and omega 3 fatty acids in their blood had better performance on mental acuity tests and less of the brain shrinkage typical of Alzheimer's disease - while "junk food" diets produced just the opposite result.

The study was among the first of its type to specifically measure a wide range of blood nutrient levels instead of basing findings on less precise data such as food questionnaires, and found positive effects of high levels of vitamins B, C, D, E and the healthy oils most commonly found in fish.

Treatment that increases brain levels of an important regulatory enzyme may slow the loss of brain cells that characterizes Huntington's disease (HD) and other neurodegenerative disorders. In a report receiving advance online publication in Nature Medicine, a Massachusetts General Hospital (MGH)-based research team reports that increased expression of Sirt1, one of a family of enzymes called sirtuins, in the brain of a mouse model of HD protected against neurodegeneration. They also identified a potential mechanism for this protective effect.

New research suggests that, in people who don't currently have memory problems, those with smaller regions of the brain's cortex may be more likely to develop symptoms consistent with very early Alzheimer's disease. The study is published in the December 21, 2011, online issue of Neurology®, the medical journal of the American Academy of Neurology.

"The ability to identify people who are not showing memory problems and other symptoms but may be at a higher risk for cognitive decline is a very important step toward developing new ways for doctors to detect Alzheimer's disease," said Susan Resnick, PhD, with the National Institute on Aging in Baltimore, who wrote an accompanying editorial.

Many people with dementia don't realize they have the disease until it's at an advanced stage, when everyone can tell something is wrong. Other people might start forgetting dates or names and worry they have dementia, yet their memory problems are just a normal consequence of aging. Having primary care doctors routinely screen patients for dementia at annual check up visits just like they do for high blood pressure or cholesterol could identify people in need of dementia care and reassure those who are healthy. That's what dementia experts argued at a meeting held last month in New York City, as reported on Alzforum.