Alzheimer's disease is the most frequent age-related neurodegenerative disorder. It is in part caused by the presence of microscopic lesions in the brain called amyloid plaques, which are composed of a peptide called amyloid beta (Aβ). Although naturally present in the brain, Aβ can accumulate over years under the influence of genetic and environmental factors to ultimately form the amyloid plaques, which are toxic for neurons.

Current research is mostly focused on cerebral amyloids. However, these aggregates are also present in the blood and in other organs. Although still controversial, blood amyloids could be of use for the diagnosis of brain pathologies.  Researchers at MIRCen studied Aβ modifications in the sera of mouse lemurs (Microcebus murinus), a type of small primate. Mouse lemurs can spontaneously present cerebral lesions comparable to those observed in patients with Alzheimer's disease. The team found that aging mouse lemurs show an increase in serum Aβ levels. These animals are also known for their seasonal behavioral changes, with notably an increase in activity in summer. The team thus looked at serum Aβ in the lemurs as a function of seasons and found a strong reduction of Aβ levels in summer. Their results suggest that, contrary to current opinion, Aβ concentrations can strongly fluctuate over time and that their regulation is visible not only in the brain but also in the blood. Further studies are needed to uncover the mechanisms driving the seasonal changes in Aβ levels. Once understood, those mechanisms could serve as a foundation for the development of a blood test for Alzheimer's disease or even new therapies.