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. UCLA neurology professor Paul Thompson and his colleagues measured levels of transferrin, a protein that transports iron throughout the body and brain, in adolescents and discovered that these transferrin levels were related to detectable differences in both the brain's macro-structure and micro-structure when the adolescents reached young adulthood.
Compared to similar people who don't take them, nursing home residents with dementia who take average doses of a class of drugs used to treat depression are three times more likely to have an injurious fall. These are the findings of a new study from The Netherlands published online in the British Journal of Clinical Pharmacology on Wednesday. Falls are a serious health problem for nursing home residents with dementia, particularly as one-third of all falls in such establishments result in injury. (In this study, the researchers noted an average rate of 3 falls per resident with dementia per year). Many nursing home residents with dementia also have depression. The type of drug most commonly prescribed for them is a class of antidepressants known as serotonin reuptake inhibitors (SSRIs).
The way in which Alzheimer's Disease spreads in the brain has been the subject of debate for many years. Two opposing theories have the disease starting independently in weakened brain regions over time, or it beginning in one region and then spreading neuroanatomically connected areas. A study published by Columbia University Medical Center (CUMC) researchers, in the online journal PloS One, strongly supports the second theory. Scientists have demonstrated that abnormal tau protein, a key feature of the neurofibrillary tangles seen in the brains of those with Alzheimer's, is able to propagate along linked brain circuits, "jumping" from neuron to neuron. Senior author Karen E. Duff, PhD, professor of pathology (in psychiatry and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute, says that the findings open new opportunities for obtaining a deeper understanding of Alzheimer's and other neurological diseases, as well as for developing therapies to halt its progression, according to senior author Karen E.
In the images of fruit flies, clusters of neurons are all lit up, forming a brightly glowing network of highways within the brain. It's exactly what University at Buffalo researcher Shermali Gunawardena was hoping to see: It meant that ORMOSIL, a novel class of nanoparticles, had successfully penetrated the insects' brains. And even after long-term exposure, the cells and the flies themselves remained unharmed. The particles, which are tagged with fluorescent proteins, hold promise as a potential vehicle for drug delivery. Each particle is a vessel, containing cavities that scientists could potentially fill with helpful chemical compounds or gene therapies to send to different parts of the human body. Gunawardena is particularly interested in using ORMOSIL - organically modified silica - to target problems within neurons that may be related to neurodegenerative disorders including Alzheimer's disease.
More than half of all cases of dementia in the elderly can be attributed to Alzheimer's disease. Despite vast research efforts, an effective therapy has not been developed, and treatment consists of dealing with the symptoms. Changes in brain tissues are a hallmark of Alzheimer's. In affected individuals, small protein fragments known as amyloid beta peptides accumulate and are deposited in the gray brain matter. Researchers recently identified a series of synthetic compounds (inhibitors) that interfere with the self-assembly of the amyloid beta peptide in vitro; they influence both early stages and the transition to the characteristic amyloid fibrils. On a theoretical level, these compounds thus satisfy an initial condition for the development of an Alzheimer drug. Peptide's disorder determines interaction In order to understand the interactions between the amyloid beta peptide and active compounds at a structural level, Marino Convertino, Andreas Vitalis, and Amedeo Caflisch from the University of Zurich's Department of Biochemistry simulated these interactions on the computer.