New hope in untangling Alzheimer’s Disease

“Our biggest hope is to be able to one day use microRNAs to detect Alzheimer’s disease in people at a young age and begin treatment based on our findings.”

A team of Tel Aviv University researchers have identified a specific set of molecules called microRNAs that detrimentally regulate protein levels in the brains of mice with Alzheimer’s disease


and beneficially regulate protein levels in the brains of other mice living in a stimulating environment.

“We were able to create two lists of microRNAs — those that contribute to brain performance and those that detract — depending on their levels in the brain,” says Dr. Boaz Barak, one of the authors of the study. “By targeting these molecules, we hope to move closer toward earlier detection and better treatment of Alzheimer’s disease.”

The researchers ran a series of tests on a part of the mice’s brains called the hippocampus, which plays a major role in memory and spatial navigation and is one of the earliest targets of Alzheimer’s disease in humans. They found that, compared to mice in normal cages, the mice from the living in an “enriched environment” — an enlarged cage with running wheels, bedding and nesting material, a house, and frequently changing toys — developed higher levels of good proteins and lower levels of bad proteins.

For the first time, Barak and a team of researchers in the lab of Prof. Uri Ashery of Tel Aviv University’s Department of Neurobiology at the George S. Wise Faculty of Life Sciences and the Sagol School of Neuroscience identified the microRNAs responsible for regulating the expression of both good and bad proteins.

Prof. Daniel Michaelson of TAU’s Department of Neurobiology in the George S. Wise Faculty of Life Sciences and the Sagol School of Neuroscience, Dr. Noam Shomron of TAU’s Department of Cell and Developmental Biology and Sagol School of Neuroscience, Dr. Eitan Okun of Bar-Ilan University, and Dr. Mark Mattson of the National Institute on Aging collaborated on the study, published in Translational Psychiatry.

Two findings appear to have particular potential for treating people with Alzheimer’s disease. In the brains of old mice with the disease, microRNA-325 was diminished, leading to higher levels of tomosyn, a protein that is well known to inhibit cellular communication in the brain. The researchers hope that eventually microRNA-325 can be used to create a drug to help Alzheimer’s patients maintain low levels of tomosyn and preserve brain function.

The researchers also found several important microRNAs at low levels starting in the brains of young mice. If the same can be found in humans, these microRNAs could be used as biomarker to detect Alzheimer’s disease at a much earlier age than is now possible — at 30 years of age, for example, instead of 60.

“Our biggest hope is to be able to one day use microRNAs to detect Alzheimer’s disease in people at a young age and begin a tailor-made treatment based on our findings, right away,” says Dr. Barak.

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About Viva Sarah Press

Viva Sarah Press is an associate editor and writer at ISRAEL21c. She has extensive experience in reporting/editing in the print, online and broadcast fields. Her work has been published by international media outlets including Israel Television, CNN, Reuters, The Jerusalem Post and Time Out.
  • Charlene

    My maternal side of the family needed that. Some had alzheimers, and some like my mother had dementia. Many of her aunts had alzheimers. Her baby brother who is 87 now has suffered the past seven years very noticeably, and even tho on aricept and another medication, he is now like a sweet compliant child who says he is being taken care of by a woman he knows loves him very much (his wife). He can’t always get dressed or get to the bathroom but still makes the bed and dries the dishes. he looks about 70′ played golf his whole life literally, and can usually beat anyone at a game of cards (clabber) when my aunt has their Wednesday lunch and card game at their home.

    As I have watched my mother and her siblings, each had their memory problem kicked off by an incident which affected or seemed to have brought it out. Momma had mini strokes and then several larger ones, leaving minimal visible damage but the demntia. Aunt had brain injury in 1948 and about in sometime around 2000 after her dog died, she flipped badly and became highly entertaining as my brother would say, she died 6 years ago a mental disaster. brother after passing a clot after heart surgery came home and lived a normal life until he went for milk one Christmas eve in Southern Ind and was found in Lansing MI 3 weeks later totally disoriented and died days later. The baby brother had his kicked off visibly when his blood pressure medication dropped his BP so much that he passed out