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Pathologically, the brainstem locus coeruleus (LC), the main source of the neurotransmitter noradrenalin (NA) modulating olfactory information processing is affected early. Here we show early and distinct loss of noradrenergic input to the olfactory bulb (OB) coinciding with impaired olfaction in an AD mouse model, before appearance of amyloid plaques. Mechanistically, OB microglia recognize and phagocytose LC axons. Reducing phagocytosis genetically preserves LC axons and olfaction. Prodromal AD patients display elevated TSPO-PET signals in the OB, similarly to                     <jats:italic>App</jats:italic>                     <jats:sup>                       <jats:italic>NL-G-F</jats:italic>                     </jats:sup>                     mice. We further confirm early LC axon degeneration in post-mortem OBs in patients with early AD. 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