News of Note—How an Alzheimer’s gene may cause memory loss; a nanoparticle flu vaccine

The gene variant ApoE4 impacts the complexity of dendrites extending from adult-born neurons in mice, possibly contributing to Alzheimer's risk, scientists have discovered. (NICHD/S. Jeong)

New insight into Alzheimer’s risk gene

The gene variant Apolipoprotein E4 (ApoE4) is a known risk factor for late-onset Alzheimer’s disease. Now researchers at Columbia University in New York have demonstrated a key role of ApoE in the proper development of neurons that form in the adult brain—a discovery that may help explain why people with the mutation face a high risk of Alzheimer’s. They found that the dendrites extending from adult-born neurons in mice without ApoE or with ApoE4 were less complex than those in unaltered mice, which they believe may contribute to memory loss. They published their findings in the journal eNeuro. (Release)

Nanoparticle vaccine protects mice from several flu viruses

Researchers led by Georgia State University have developed a flu vaccine made of double-layered peptide nanoparticles, which is designed to provide broad flu protection by touching off T-cell immune responses. The nanoparticle is coated with four peptides that are contained in most influenza A viruses. In a study published in the Proceedings of the National Academy of Sciences, the researchers used a microneedle patch to deliver the vaccine to mice. All of the mice that received the vaccine survived a variety of flu exposures, while those given a placebo did not, they reported. (Release)

Newly identified gene could improve RA treatment

A team at the Icahn School of Medicine at Mount Sinai in New York has discovered a gene that’s predictive of the severity of rheumatoid arthritis. They focused on “synovial fibroblasts,” which are cells inside of joints. Working with rodent models, they pinpointed a DNA region containing 41 genes that control arthritis severity and joint damage. After sequencing those genes, they discovered that a mutation in a gene called HIP1 controls the behavior of synovial fibroblasts, which proliferate and become invasive in people with RA. They went on to discover that mice deficient in HIP1 developed a milder form of arthritis. They believe their findings, published in the journal Annals of the Rheumatic Diseases, raise the possibility of targeting HIP1 in the treatment of RA. (Release)

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