Establishing a Biophotonic Signature of Brain Ageing.
4 affiliations
- 1School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia.
- 2Institute of Veterinary Physiology and Biochemistry, Justus Liebig, University Giessen, Giessen, Germany.
- 3Department of Biochemistry, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
- 4Department of Physics, School of Science, RMIT University, Melbourne, Victoria, Australia.
Abstract
Ageing-associated inflammation ("inflammaging") is characterised by chronic microglial priming or overactivity that elevates neurodegeneration risk. Microglia also accumulate autofluorescent lipofuscin as they age-aggregates of oxidised lipids, misfolded proteins and metals that generate reactive oxygen species. Characterising age-related changes in brain autofluorescence could provide insight into brain ageing dynamics and could identify associations with potential biomarkers in accessible tissues such as blood. We hypothesised that the ageing-related increase in microglial autofluorescent material produces a spectral signature that makes ageing autofluorescence distinct from that in young brains. To test this, we examined autofluorescence profiles in the hippocampus and arcuate nucleus (ARC) of young (3 months) and aged (21 months) female C57BL/6 mice. We found that ageing significantly increased the volume of the autofluorescent material in microglia, including driving an abundance of extra-large aggregates. In the ARC, larger aggregates-present only in aged brains-exhibited stronger far-red emission than the autofluorescence seen in young brains. Fluorescence lifetime imaging analysis indicated specific ageing-related molecular changes in brain autofluorescence. Lipidomic analysis from the plasma of these mice indicated 22 lipids that were differentially concentrated with age and one (sphingomyelin 32:2) that was significantly associated with the ageing brain spectral profile after controlling for multiple comparisons and validating in a separate cohort. These findings demonstrate that autofluorescent material aggregates with age in microglia and that brain autofluorescence undergoes a spectral red-shift associated with ageing and lipid alterations. Brain autofluorescence may thus reflect brain ageing with potential translational relevance for non-invasive monitoring.
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BibTeX
@article{slayo2026establishing,
title = {{Establishing a Biophotonic Signature of Brain Ageing.}},
author = {Mary Slayo and Loretta Vocale and Soniya Xavier and Pasindu Singhaarachchi and Kylie M Quinn and Blanca Del Rosal and Sarah J Spencer},
journal = {Aging cell},
year = {2026},
month = nov,
doi = {10.1111/acel.70790},
url = {https://europepmc.org/article/MED/42967488},
note = {CC BY},
}
RIS
TY - JOUR
TI - Establishing a Biophotonic Signature of Brain Ageing.
AU - Mary Slayo
AU - Loretta Vocale
AU - Soniya Xavier
AU - Pasindu Singhaarachchi
AU - Kylie M Quinn
AU - Blanca Del Rosal
AU - Sarah J Spencer
PY - 2026
DA - 2026/11/01
JO - Aging cell
DO - 10.1111/acel.70790
UR - https://europepmc.org/article/MED/42967488
AB - Ageing-associated inflammation ("inflammaging") is characterised by chronic microglial priming or overactivity that elevates neurodegeneration risk. Microglia also accumulate autofluorescent lipofuscin as they age-aggregates of oxidised lipids, misfolded proteins and metals that generate reactive oxygen species. Characterising age-related changes in brain autofluorescence could provide insight into brain ageing dynamics and could identify associations with potential biomarkers in accessible tissues such as blood. We hypothesised that the ageing-related increase in microglial autofluorescent material produces a spectral signature that makes ageing autofluorescence distinct from that in young brains. To test this, we examined autofluorescence profiles in the hippocampus and arcuate nucleus (ARC) of young (3 months) and aged (21 months) female C57BL/6 mice. We found that ageing significantly increased the volume of the autofluorescent material in microglia, including driving an abundance of extra-large aggregates. In the ARC, larger aggregates-present only in aged brains-exhibited stronger far-red emission than the autofluorescence seen in young brains. Fluorescence lifetime imaging analysis indicated specific ageing-related molecular changes in brain autofluorescence. Lipidomic analysis from the plasma of these mice indicated 22 lipids that were differentially concentrated with age and one (sphingomyelin 32:2) that was significantly associated with the ageing brain spectral profile after controlling for multiple comparisons and validating in a separate cohort. These findings demonstrate that autofluorescent material aggregates with age in microglia and that brain autofluorescence undergoes a spectral red-shift associated with ageing and lipid alterations. Brain autofluorescence may thus reflect brain ageing with potential translational relevance for non-invasive monitoring.
SN - 1474-9718
SN - 1474-9726
ER -