Funded by a two-year, nearly $350,000 grant from the National Institutes of Health’s National Institute on Aging, the University of Cincinnati’s Shawn Xiong, PhD, is analyzing real-world patient data to learn more about how GLP-1 drugs affect people with mild cognitive impairment, a common precursor to Alzheimer’s disease.

A team led by Dr. Kuan-lin Huang, PhD, has been named a winner of the $1 million Alzheimer’s Insights AI Prize, the Alzheimer’s Disease Data Initiative (AD Data Initiative) announced on March 20. Dr. Huang is an Associate Professor of Genetics and Genomic Sciences at the Icahn School of Medicine at Mount Sinai. The award honors the development of Biomni-AD, an advanced AI-powered “co-scientist” designed to dramatically reduce the time required to generate scientific insights from complex biomedical data. The Mount Sinai team collaborated with partners at Stanford University on the winning project. Originally conceived as a single $1 million award, the competition expanded to recognize two winning teams, doubling the total prize amount to $2 million—reflecting both the exceptional quality of submissions and the urgency of advancing new approaches to Alzheimer’s disease and related dementias.

A summary of the presentations and findings of the International Conference on Nutrition in Medicine (ICNM), the annual meeting conducted by the Physicians Committee for Responsible Medicine, was published today in the International Journal of Disease Reversal and Prevention. Clinicians now have ready access to the latest information regarding the role of dietary interventions in breast and prostate cancers, menopause, and Alzheimer’s disease, among others.

Down syndrome (DS), caused by trisomy 21 (T21), affects approximately 1 in 700 live births and is characterized by a wide spectrum of features, including cognitive impairment, craniofacial abnormalities, congenital heart defects, and early-onset Alzheimer disease (EOAD). Among the ~364 protein-coding genes triplicated on HSA21, DYRK1A (dual-specificity tyrosine phosphorylation-regulated kinase 1A) has emerged as a key contributor to neurodevelopmental deficits. This review summarizes the neurogenetic consequences of DYRK1A triplication, its interactions with other genes, and therapeutic strategies targeting its overexpression.