A new drug could reduce memory loss in mice with Alzheimer's disease.
Researchers at California's Salk Institute have found a drug that changes the way brain cells metabolize certain fats, reducing memory loss in mice with Alzheimer's disease.
Based on a chemical called fisetin found in fruits and vegetables, the new drug — called CMS121 — slowed the degeneration of brain cells in mice.
The researchers, led by senior staff scientist Pamela Maher, dosed mice who had inherited Alzheimer's disease with CMS121 at a point akin to middle age in humans and after the mice had already begun to show learning and memory problems, according to a report from the Salk Institute. The scientists published their work in the journal Redox Biology.
Mice dosed with the drug performed as well as healthy mice in memory and behavior tests after three months.
The drug is thought to work by degrading the fatty molecules called lipids that cause cell damage in the brain. Maher and her team are looking to begin clinical trials of CMS121, as well as similar compounds using the same target.
"There has been a big struggle in the field right now to fund targets to go after," Maher said. "So identifying a new target in an unbiased way like this is really exciting and opens lots of doors."
Alzheimer's disease is a notoriously difficult condition to treat. Pharmaceutical companies like Biogen Inc., Eli Lilly and Co., Roche Holding AG and others that have pursued medicines to heal the damage caused by the disease have encountered many hurdles along the way.
Antibiotics and the 'social brain'
The microbiome is made up of the many different microbes within a living body, and the interactions within that system play a role in biological function.
Researchers from the University of Oxford have found that in young mice who are treated with antibiotics — reducing the number of microbes in their system — certain chemicals that dictate social and behavioral function can be altered.
"Our research underlines the growing consensus that disturbing the microbiome during development can have significant impacts on physiology, including the brain," researcher Philip Burnet said in an Oxford report.
Treating the mice with high doses of antibiotics reduced the expression of receptors that signal endorphin, oxytocin and vasopression in the frontal cortex of the brain. The study could also reveal interactions between opioid receptors in the brain and the microbiome.
"The adverse effect of antibiotics on the endorphin system may have implications not only for social behavior but also for pain regulation," researcher Katerina Johnson said. "In fact, we know that the gut microbiome affects the pain response so this might be one of the ways in which it does so."
The scientists published their findings in the journal BMC Neuroscience.
Female mosquitoes can bite and spread disease, while their male counterparts cannot.
Bite-free mosquitoes through genetics
Scientists at the Virginia Polytechnic Institute have used a gene change to convert female mosquitoes into non-biting males in a study that could have implications for controlling mosquito-borne diseases.
The researchers inserted a male-determining gene into female mosquitoes, which was enough to convert the insects to the male sex. They published their findings in the journal The Proceedings of the National Academy of Sciences.
They also found that the new gene was passed down to offspring.
"Nix-mediated sex conversion was found to be highly penetrant and stable over many generations in the laboratory, meaning that these characteristics will be inherited for generations to come," Pirbright Institute senior research scientist Michelle Anderson said in a Virginia Tech report.
The added gene, however, also contributes to a lack of flight ability for the male mosquitoes, making reproduction only possible in a lab setting.
"One of the challenges is to produce transgenic lines that convert females into fertile, flying male mosquitoes by inserting both the Nix and myo-sex genes into their genome together," researcher Zach Adelman said.