Alzheimer’s disease and dementia may be more common in women with polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS), according to a review of existing evidence published in the Journal of the Endocrine Society.

A large global study provides new evidence supporting the use of blood biomarkers in an Alzheimer’s clinical trial to screen for elevated brain amyloid levels among potential participants who are cognitively unimpaired. The findings, published in JAMA Neurology, show that the relationship between the blood biomarker %p-tau217 and brain amyloid was largely similar across racial groups. The study also revealed that levels of the biomarker were generally lower among Asian and Black participants compared with White participants, and Hispanic participants compared with non-Hispanic participants. These differences raise questions about the factors that influence blood biomarker levels and how they relate to dementia risk across populations. The study included data from 15,612 adults, ages 55 to 80, collected at 106 research sites across Asia, Australia, Europe and North America. Participants were cognitively unimpaired and undergoing screening for the AHEAD 3-45 trials, which are testing lecanemab in people with certain levels of amyloid in the brain but no symptoms of Alzheimer’s disease. Participants underwent blood-based screening before eligible individuals proceeded to additional assessments, including PET scans. Although %p-tau217 levels differed across racial and ethnic groups, the marker showed similar relationships with Alzheimer’s-related measures across racial groups. Across the groups studied, higher %p-tau217 levels were consistently associated with higher levels of brain amyloid measured on PET scans. The study also found that carriers of the APOE ε4 variant, a major genetic risk factor for Alzheimer’s, generally had higher levels of %p-tau217 than adults without the variant—a pattern that largely held across racial and ethnic groups.

Regularly volunteering or informally helping people outside one’s home may buffer against accelerated decline in memory and thinking for people with a major genetic risk factor for Alzheimer’s disease. The association was strongest among people at the highest genetic risk for Alzheimer’s.

Researchers at the University of Colorado Anschutz and Pacific Northwest National Laboratory have found a new clue that may help explain why some people are more likely to develop Alzheimer’s disease. It suggests that a protein linked to the disease can change how the brain’s immune cells handle fat and trigger inflammation. Those changes could help explain how a well-known genetic risk factor for Alzheimer’s affects the brain.

A research “super team” co-led by the Buck Institute for Research on Aging and Georgetown University has received an award of up to $51.7 million from the Advanced Research Projects Agency for Health (ARPA-H) to predict how disease-causing proteins misfold before irreversible damage occurs and use those predictions to develop novel diagnostics and treatments. The four-year effort is expected to lead to new ways of detecting, slowing and treating neurodegenerative diseases and cancer, with an initial focus on Alzheimer's disease and Ewing sarcoma.

IMPEDE, a seven-institution team led by Carolina with industry partner Siemens Healthineers, aims to deliver an FDA-ready early-detection biomarker and preclinical treatments for Alzheimer’s disease and pulmonary fibrosis in just a few years.