Researchers double the number of genes known to influence Alzheimer’s disease, while a rare childhood disorder could help identify new preventative treatments.

Scientists are regularly making breakthrough discoveries in the fight against Alzheimer’s. Three new studies are helping determine a person’s genetic risk of developing the disease later in life, as well as opening new avenues for effective treatments.

A study in the journal Nature Genetics examined the genes of 74,046 people in 15 countries involved in the International Genomics of Alzheimer’s Project—the largest Alzheimer’s study ever.

Using that data, researchers found 11 genes associated with Alzheimer’s, doubling the number of genes known to be linked to the neurodegenerative disorder, which affects more than five million Americans.

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These genes could perhaps be targeted with new therapies to slow the progression of late-onset Alzheimer’s, which is the most common form of dementia.

Besides the now 22 genes associated with Alzheimer’s, researchers say that the new study identified 13 other genes that are worth investigating.

A separate study released on Monday in the journal Nature Neuroscience says that children born with A-T disease—a rare genetic disorder present in an estimated 1 in 40,000 births—may also provide a better understanding of Alzheimer’s.

Researchers at Rutgers University were the first to examine the role of the regulatory protein EZH2 in the mature nerve cells of the brain. EZH2 helps determine which genes are switched on during brain development.

Children with A-T disease suffer from mutations in their ATM gene and cannot make healthy, functioning ATM proteins. This can cause problems with coordination, equilibrium, movement, and muscle control.

Using studies of both mouse and human brain tissue, the Rutgers team found that without ATM production, levels of EZH2 increase. Upon further inspection in mouse models, researchers discovered that elevated EZH2 levels contributed to the same neuromuscular problems caused by A-T. Researchers say they were able to “cure” mice with A-T disease by increasing the levels of EZH2 in their brains.

While researchers hope their work will someday lead to new treatments for A-T disease, their larger goal is to better understand other diseases like Alzheimer’s and Parkinson’s and determine what role, if any, EZH2 plays in their development.

“On a larger level, this research provides a strong clue toward understanding more common neurodegenerative disorders that may use similar pathways,” Prof. Ronald Hart of the Rutgers University Department of Cell Biology and Neuroscience, said in a statement. “It is a theme that has not yet been examined.”

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Researchers at Tel Aviv University released findings on Monday about two proteins they say are worthy of future research.

Scientists there say they’ve found two lists of microRNAs—small molecules that affect gene expression—with the potential to treat Alzheimer’s. Both contribute to brain performance, depending on how much of them there is in the brain.

In the brains of old mice with Alzheimer’s, researchers found that microRNA-325 was diminished. This led to higher levels of tomosyn, a protein that inhibits communication between cells in the brain. Researchers hope new therapies targeting this protein could help Alzheimer’s patients preserve their brain function.

Besides the relationship between microRNA-325 and tomosyn, researchers found other microRNAs at low levels in young mice, which could be used as a biomarker for Alzheimer’s. This might mean that risk assessments for dementia could begin at age 30, not age 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,” Dr. Boaz Barak of Tel Aviv’s Department of Neurobiology said in a statement.