Autofluorescence from mouse brain tissue shifts measurably toward the red end of the spectrum with age, driven by accumulation of large lipofuscin aggregates within microglia in the hippocampus and arcuate nucleus. A single circulating lipid, sphingomyelin 32:2, tracked this spectral signature and was validated in a separate cohort, pointing toward a blood-accessible correlate of brain ageing. The work establishes an optical readout of neuroinflammatory ageing that may eventually support non-invasive monitoring.
Key Points
- Aged brain autofluorescence red-shifts; young brain autofluorescence stays blue-shifted
- Microglial lipofuscin aggregates grow larger and more abundant with age
- Plasma sphingomyelin 32:2 predicts the ageing spectral signature
Longevity Analysis
Lipofuscin accumulation represents the visible residue of failed cellular clearance — oxidised lipids, misfolded proteins and metals that resident immune cells of the brain can no longer break down. Linking that intracellular debris to a measurable spectral property and then to a single circulating lipid narrows the gap between slow neuroinflammatory decline and something that can be tracked from a blood draw. Interventions aimed at waste disposal, oxidative load and glial activation currently lack early readouts in living tissue; a signal of this kind would allow the effect of such strategies to be observed long before cognitive symptoms appear.
Original published by Wiley Aging Cell, by Mary Slayo, Loretta Vocale, Soniya Xavier, Pasindu Singhaarachchi, Kylie M. Quinn, Blanca del Rosal, Sarah J. Spencer .