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Previous research has shown that levels of the protein sTREM2 in cerebrospinal fluid (CSF) decrease in the early stages of Alzheimer’s disease (AD) compared with cognitively normal individuals; however, these sTREM2 levels are higher than normal in late-stage AD. The role of these fluctuations in AD progression is unknown. An international group of researchers, led […]

Researchers at Columbia University Vagelos College of Physicians and Surgeons, including FunGen-AD researchers Badri Vardarajan and Richard Mayeux, have identified a previously unknown genetic variant that can reduce an individual’s odds of developing Alzheimer’s disease (AD).

International researchers, including FunGen-AD researcher Philip De Jager, teamed up to explore the effects of genetic variants on expression in specific cell types and subtypes in the brains of older individuals.

FunGen-AD researcher Alison Goate was part of a team of researchers at the Icahn School of Medicine at Mount Sinai that used genetic and genomic tools to uncover new information about regulators of the macrophage transcriptomic state. These discoveries could provide therapeutic targets for modulating macrophage function in Alzheimer’s and other diseases.

Genetic studies have linked variations of the SORL1 gene to both early- and late-stage Alzheimer’s disease (AD), but the exact link between damaged SORL1 genes and AD was not previously known. To further understand the role of SORL1 in AD, a team of researchers—including FunGen-AD grantee Philip L. De Jager—analyzed stem cells from patients with AD.

FunGen-AD grantee Peter St George-Hyslop was part of a collaboration among researchers from the University of Sydney, University of Cambridge, Harvard University, and Columbia University that developed new optical methods to observe development of pathological protein aggregates in cells.

FunGen-AD investigator Carlos Cruchaga and a team of researchers at Washington University School of Medicine in St. Louis analyzed proteins in brain tissue, cerebrospinal fluid (CSF), and plasma samples from patients with sporadic Alzheimer’s Disease (AD) or autosomal dominant AD, TREM2 variant carriers, and healthy individuals.