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New research from SAHMRI has found a link between the omega-3 fatty acid known as docosahexaenoic acid (DHA) and increased IQ among children born prematurely.

Preterm children are more likely to have lower IQ scores and cognitive impairments compared with term-born children.

Dr. Jacqueline Gould, who led the study now published in the New England Journal of Medicine, says infants born at the earliest gestations are deprived of the natural supply of DHA that normally builds up in the brain during the last trimester of pregnancy.

Biomedical and electrical engineers at UNSW Sydney have developed a new way to measure neural activity using light—rather than electricity—which could lead to a complete reimagining of medical technologies like nerve-operated prosthetics and brain-machine interfaces.

Professor François Ladouceur, with UNSW’s School of Electrical Engineering and Telecommunications, says the multi-disciplinary team has just demonstrated in the lab what it proved theoretically shortly before the pandemic: that sensors built using liquid crystal and integrated optics technologies—dubbed “optrodes”—can register nerve impulses in a living animal body.

Not only do these optrodes perform just as well as conventional electrodes—that use electricity to detect a nerve impulse—but they also address “very thorny issues that competing technologies cannot address,” says Prof. Ladouceur.

Understanding the neural mechanisms of conscious and unconscious experience is a major goal of fundamental and translational neuroscience. Here, we target the early visual cortex with a protocol of noninvasive, high-resolution alternating current stimulation while participants performed a delayed target–probe discrimination task and reveal dissociable mechanisms of mnemonic processing for conscious and unconscious perceptual contents. Entraining β-rhythms in bilateral visual areas preferentially enhanced short-term memory for seen information, whereas α-entrainment in the same region preferentially enhanced short-term memory for unseen information. The short-term memory improvements were frequency-specific and long-lasting. The results add a mechanistic foundation to existing theories of consciousness, call for revisions to these theories, and contribute to the development of nonpharmacological therapeutics for improving visual cortical processing.

The overexpression of a gene tied to cell division and the structure and function of neurons may prevent and protect against cognitive decline in both mice and humans with Alzheimer’s disease (AD), according to a new study by scientists at the University of Colorado Anschutz Medical Campus.

The gene, Kinesin-5 or KIF11, does this despite the presence of amyloid beta (Abeta), the main component of plaques in the brains of those with AD. Scientists have traditionally targeted the plaques when looking for treatments for the fatal disease. In this case, they went around them.

The study was published online last week in the journal iScience.

If you thought it was easy to analyze brain cells, think again.

When you take a brain tissue sample, all that your analysis would normally show you is an average for all the present. And since there are a whole lot of cell types in our brain— and others—you’ll get a sort of cell smoothie, which makes it difficult if not impossible to tell the cells apart, let alone study them.

It is like wanting to know how many green M&M’s there are in a bowl, but instead just getting told how many colors there are. You are not really getting the answer you wanted.

New imaging of patients with Alzheimer’s demonstrates how a telltale protein spreads throughout the brain based on the phenotype of the disease, i.e., whether the condition is dominated by forgetfulness, or atrophy in a specific brain region. The research offers a host of illuminating clues that ultimately may inform new treatment strategies.

The protein is known as tau and a large multi-disciplinary team of brain researchers at McGill University in Montreal has been able to trace the protein’s patterns in living patients via magnetic resonance imaging (MRI). Alzheimer’s disease is intimately linked to tau, which can form tangles in the brain that irrevocably damage neurons.

The patterns detected by McGill scientists apparently are unique to the phenotype of Alzheimer’s afflicting the patient. This staggering finding opens an intriguing new window into the molecular mechanisms of the disease. And while many features of Alzheimer’s are the same from one patient to the next, phenotypes are a hallmark of the condition. Tracking tau patterns is a specialty of the scientists at McGill, who found that the intrinsic connectivity of the human brain itself provides the scaffolding for the aggregation of tau in distinct variants of the disease.