Alzheimer disease (AD) is a common neurodegenerative disorder with multiple facets. Many research questions have been raised since the first description of AD. Starting from a neuropathological point of view, the respective roles of the two hallmarks of AD, namely extra-cellular senile plaques centered by amyloid-β aggregates, and intra-neuronal neurofibrillary tangles, composed of hyperphosphorylated Tau protein, have long been a matter of debate. From a clinical point of view, the very broad range of ages at first symptoms (age of onset, AOO), from the early twenties to supercentenarians, as well as clinical diversity among patients, is also a source of research questions. Understanding the etiology of AD can provide critical insights into many of these questions. Epidemiological studies suggest that genetic factors play a substantial role in AD etiology [1], in addition to rare families with autosomal dominant inheritance. Strongest genetic factors, i.e. those associated with the highest probabilities of developing AD for a carrier, bring important insights into disease etiology, while modest risk factors, which are only slightly more common in patients than in unaffected controls, can be both etiological factors with a low effect or facilitators of the pathophysiology, at any stage and not necessarily upstream of it-

In this review, I will provide an overview of the current knowledge in AD genetics, both in the field of strong determinants of AD risk, starting with pathogenic variants in Mendelian genes, to the recent discovery of multiple risk factors with a wide range of associated levels of risk.