Katrin I. Andreasson
Stanford University, CA·Neuroscience
Why does the aging brain become more vulnerable to memory loss and Alzheimer's disease (AD)? These projects focus on myeloid cells, immune cells that include microglia (the brain's resident immune cells) and the monocytes and macrophages that circulate in the blood and body.
- Fields
Neuroscience
Microbiology & Immunology
Medicine & Clinical Research
- Topics
Alzheimer's disease
cognitive aging
neuroinflammation
- Grants
- 3 known grants, through Jan 2028
What they work on
- Test whether reprogramming energy metabolism in aging microglia and blood macrophages, by blocking inflammatory PGE2 signaling, can prevent or reverse cognitive decline in aging and Alzheimer's model mice.
- Determine whether brain or body myeloid cells drive the metabolic deficits linked to brain aging, and whether targeting myeloid metabolism is a viable therapeutic approach for Alzheimer's disease.
- Test whether blocking the PGE2 receptor EP2 only outside the brain reprograms circulating blood cells to improve the function of brain blood-vessel lining cells, using aging and mutant APP mice with metabolomics and transcriptomics.
- Determine whether peripheral EP2 inhibition improves how astrocytes, support cells wrapping brain capillaries, fuel neurons, and whether this restores hippocampal function and memory in aging and Alzheimer's models.
- Separate the effects of blood immune cells from those of brain microglia on age- and amyloid-related cognitive decline, using a new bone marrow transplantation approach and genetic targeting of microglia.
- Define how the TREM1 immune receptor pathway acts in body and brain myeloid cells to affect cognition through immune-metabolic mechanisms, and determine TREM1's function in human myeloid cells.
More about the research
With age, these cells shift toward harmful, long-lasting inflammation. Human genetic studies point to faulty myeloid cells as a major AD risk factor. The work asks whether immune cells in the brain, in the body, or both drive cognitive decline. It also asks whether fixing how these cells produce energy could protect memory.
Why it matters
Age-related cognitive decline and Alzheimer's disease affect a very large number of older adults, and few treatments change the course of disease. These studies could identify immune and metabolic targets, such as the EP2 and TREM1 pathways, for disease-modifying therapies. They also test whether drugs acting on immune cells in the blood, without entering the brain, may protect memory. That could offer an easier route to treatment.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Metabolic mechanisms of cognitive decline in aging and AD mediated by inflammatory PGE2 signaling
NIH · Feb 2023 – Jan 2028
The role of peripheral versus brain myeloid immunity in the cognitive decline of aging and Alzheimer's disease
NIH · Aug 2022 – Jul 2027
Reprogramming myeloid cell metabolism to prevent cognitive aging and Alzheimer's Disease
NIH · Mar 2021 – Feb 2027
Closest labs
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Robert Tower
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The school
Stanford University: 87 labs on PI Pages, $1.6B a year on research, 739 research doctorates a year.
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