[Extract from the AEF dispatch of January 5, 2022] As part of its drive to promote “science with and for society”, on March 18, 2024 the ANR launched a new call specifically aimed at research projects it had already funded in 2021. The aim is for these winning projects to propose and implement “scientific mediation, communication or promotion actions” on their issues and results, aimed at a non-specialist audience. Submission of proposals to this call, entitled SAPS-CSTI-Générique21, is open until April 25, 2024. This call “aims to implement scientific communication, mediation and promotion actions around the issues, methods and results of research projects supported by the ANR as part of the 2021 generic project calls, under the JCJC (young researchers) and PRC (collaborative research projects) funding schemes”, states the call text. “All forms of scientific mediation, communication and promotion can be envisaged”, emphasizes the ANR. However, “they must be of a structuring nature at local, regional or national level, by jointly mobilizing the project coordinators [...] within the establishments, but also the scientific culture structures [...], and in particular those referenced by the Ocim (Office de coopération et d'information muséales)”. The aim is to create or reinforce a real synergy between scientists and professionals in the fields of scientific communication, mediation and promotion, “backed up by a steering mechanism to ensure the coherence and visibility of the actions carried out”, explains the ANR.

It is widely accepted that synaptic alteration/loss is the strongest predictor of cognitive decline in Alzheimer’s disease. However, this has mainly been based on histopathological studies in post-mortem brains which do not capture dynamic events that precede the observed synapse loss and in particular fall short in providing information on the impaired physiological function of synapses. In the PreSSAD project, we aim at addressing presymptomatic synaptic deficits in the context of the human AD pathology, by combining the expertise of five groups spanning from the identification of CSF biomarkers in preclinical AD cohorts to human synaptic biology. A major originality of the proposal is in the use of innovative human biological samples: 1) grafting human neurons with Cre-dependent null alleles for SNARE proteins in newborn mouse neocortex, 2) human induced pluripotent stem cells (iPSCs)-derived cerebral organoids and 3) viral mediated gene targeting in organotypic cortical cultures obtained from human surgical resections. All models of human neurons and circuits will be genetically targeted to assess the early physiopathological stages of synapse dysfunction and loss, in combination with a proteomic analysis of synaptic biomarkers. This project will help identifying new pre-diagnostic markers linked to altered presynaptic function in presymptomatic forms of AD.