Female-specific sex hormones can accelerate a specific type of macular degeneration that impairs the retina’s ability to sense light and eventually leads to blindness, according to new research in mice. The work identifies sex differences in retinitis pigmentosa (RP) and offers a biological explanation for why the disorder appears more frequently in females. “As sex hormones are among the most widely prescribed medications for women in the United States, there is a critical need to understand how such a widely prescribed medication affects chronic conditions and reevaluate the safety of these medications for patients with certain forms of RP and other neurodegenerative disorders,” Ashley Rowe and colleagues write. Rates of neurodegenerative conditions, such as Alzheimer’s disease (AD), differ in males and females. Here, Rowe et al. explored whether this phenomenon extends to the eyes. The team monitored eyesight decline in male and female mice with RP by performing electroretinography at each month starting at seven months of age. They found that females experienced faster neurodegeneration – an unexpected finding given that other neurodegenerative diseases tend to be more prevalent in males. Circulating female-specific sex hormones accelerated RP pathology in already-diseased neurons. Hormone depletion via ovary removal eliminated this sex difference. Meanwhile, hormone reintroduction via externally administered estradiol amplified RP progression in the female mice. When the researchers analyzed the animals’ retinas, they found females had changes to two genes for inflammatory and explosive cell death (pyroptosis) and stress-induced apoptosis.

 

For reporters eyeing discoveries related to the retinal degeneration and regeneration, as 2025 Science Translational Medicine study identified two retinal stem cell populations that could support regenerative eye therapy: www.science.org/doi/10.1126/scitranslmed.adp6864.

 

For journalists tracking sex differences in neurodegenerative diseases, the 2025 special issue in Science Advances reported on medical and societal disparities in women’s health: https://www.science.org/toc/sciadv/11/10.

Heavy drinkers who have eight or more alcoholic drinks per week have an increased risk of brain lesions called hyaline arteriolosclerosis, signs of brain injury that are associated with memory and thinking problems, according to a study published on April 9, 2025, online in Neurology^®, the medical journal of the American Academy of Neurology. The study does not prove that heavy drinking causes brain injury; it only shows an association.

While some studies have suggested that having a mother with Alzheimer’s disease may put you more at risk of developing the disease, a new study finds that having a father with the disease may be tied to a greater spread of the tau protein in the brain that is a sign of the disease, according to a study published on April 9, 2025, online in Neurology^®, the medical journal of the American Academy of Neurology. The study does not prove that having a father with Alzheimer’s results in these brain changes; it only shows an association.

ATRI Researchers have dosed the first participant in a clinical trial of an investigational medicine designed to lower the amount of amyloid precursor protein (APP) for the potential treatment of Alzheimer’s disease (AD), which is initially being studied in adults with Down syndrome (DS) who have a genetic risk of developing AD. Those with Down syndrome are born with an extra chromosome that carries a gene pivotal to causing Alzheimer’s. The gene produces a protein that causes a buildup of plaques in the brain. By the time most people with Down syndrome hit age 40, they have already developed these plaques. It may take another decade or more to develop symptoms, but eventually up to nine in 10 people with Down syndrome are expected to develop Alzheimer’s disease. Seeking to change these odds, last month, researchers gave the first dose of an investigative drug to a participant in the new clinical trial, called the HERO study. The drug is designed to stop Alzheimer’s-causing plaques from forming in the brain. Led by Ionis Pharmaceuticals, with investigative oversight by ATRI Medical Director Michael Rafii, MD, PhD, the study is expected to run for two years with an initial 30 participants at sites across the U.S. and Europe.

Tim-3 is an immune checkpoint molecule involved in immunity and inflammation recently linked to late-onset Alzheimer’s disease (AD), but its role in the brain was unknown until now. In a paper published in Nature, researchers from Mass General Brigham used preclinical models to uncover Tim-3’s role in microglia, the brain's resident immune cells, and have identified it as a promising therapeutic target for Alzheimer’s disease.