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Recent advances in neurobiology, paleontology, and paleogenetics allow us to associate changes in brain size and organization with three main “moments” of increased behavioral complexity and, more speculatively, language development. First, Australopiths display a significant increase in brain size relative to the great apes and an incipient extension of postnatal brain development. However, their cortical organization remains essentially similar to that of apes. Second, over the last 2 My, with two notable exceptions, brain size increases dramatically, partly in relation to changes in body size. Differential enlargements and reorganizations of cortical areas lay the foundation for the “language-ready” brain and cumulative culture of later Homo species. Third, in Homo sapiens, brain size remains fairly stable over the last 300,000 years but an important cerebral reorganization takes place. It affects the frontal and temporal lobes, the parietal areas and the cerebellum and resulted in a more globular shape of the brain. These changes are associated, among others, with an increased development of long-distance—horizontal—connections. A few regulatory genetic events took place in the course of this hominization process with, in particular, enhanced neuronal proliferation and global brain connectivity.

Louis Pasteur is celebrated as the founding father of microbiology. But he was a chemist by training and discovered molecular dissymmetry experimentally. All his life, his constant preoccupation will be to apply the method and strategies of the fundamental sciences to living processes, “from the molecule to the brain”. His fundamental aim will be, beyond the biology of microbes, the chemistry of life, a disposition which signs the originality of his work. More unexpectedly, Pasteur was at the origin of therapeutic chemistry—which his successors, and especially Daniel Bovet, brilliantly illustrated at the Pasteur Institute and which they would pursue with the pharmacology of the nervous system or “neuropharmacology”.

SARS-CoV-2 epidemics raises a considerable issue of public health at the planetary scale. There is a pressing urgency to find treatments based upon currently available scientific knowledge. Therefore, we tentatively propose a hypothesis which hopefully might ultimately help save lives. Based on the current scientific literature and on new epidemiological data which reveal that current smoking status appears to be a protective factor against the infection by SARS-CoV-2 [1], we hypothesize that the nicotinic acetylcholine receptor (nAChR) plays a key role in the pathophysiology of Covid-19 infection and might represent a target for the prevention and control of Covid-19 infection.