Immune-Related Protein Has Opposing Actions in Early and Late Stage Alzheimer’s in Mice

Immune-Related Protein Has Opposing Actions in Early and Late Stage Alzheimer’s in Mice
Removing a protein involved in neuroinflammation is beneficial in early stages of Alzheimer’s disease in mice. However, in late disease stages of the disease, this action has the opposite effect, according to an animal study that helps explain contradicting results observed in earlier research. The findings highlight the role of neuroinflammation in Alzheimer’s disease, and also demonstrate that different treatment approaches may be needed during various stages of the disease. The study, “Disease progression-dependent effects of TREM2 deficiency in a mouse model of Alzheimer's disease,” was published in the Journal of Neuroscience. The protein, TREM2 (triggering receptor expressed on myeloid cells 2), is found on brain immune cells. When it detects abnormalities in the brain, such as the presence of amyloid-beta plaque, it signals for immune cells to gather and handle the problem. But too fierce immune activation may also be damaging for the brain and researchers discovered that by removing TREM2 from mice, the mice fared better. However, other researchers reported that TREM2 removal was hazardous for mice with Alzheimer’s disease, as the brain suffered from the abrupt influx of cells. "Our lab and others had previously published conflicting results about how TREM2 affected pathology in Alzheimer's mouse models. One group published data showing Alzheimer's mice lacking TREM2 had more amyloid plaques. We previously found the opposite, that getting rid of TREM2 improved amyloid pathology," Taylor Jay, the study's lead author and a graduate student in the de
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