The present invention relates to the field of treat age-related cognitive declines. In this study, the inventors report that GPR158, which localizes at the PC, is required for OCN- dependent
autophagy induction in hippocampal neurons. Consistently, the mobilization of key
autophagy players by OCN in hippocampal neurons requires core PC-proteins. In aged hippocampi, neuronal PC present an abnormal morphology, correlated with a reduction of the major core ciliary proteins levels. Conversely, restoration of their levels in aged hippocampi is sufficient to improve
autophagy and cognitive deficits. Lastly, they show that core PC-proteins are required to integrate the rejuvenating effects of OCN in the
hippocampus, thereby ameliorating age-related cognitive deficits. Altogether, these findings demonstrate a new paradigm for the
neuron / systemic milieu communication and significantly advance our understanding of the regulatory mechanism mediating the rejuvenating effects of the pro-youth blood factor, OCN, in hippocampal neurons. This study also provides the foundation for novel therapeutic strategies to treat age-related
cognitive decline, as well as neurological deficits in ciliopathies. Thus, the present invention relates to an activator of the primary cilia (PC) for use in the restoration and / or improvement of cognitive functions in a subject in need thereof.