‚Neural Beschneidung‘ treibt den Geruchsverlust in frühen, stillen Stadien von Alzheimer an | Wissenschaftler entdecken bei Mäusen den Mechanismus hinter dem Geruchsverlust – der einer der ersten Indikatoren für die Alzheimer -Krankheit sein kann

From the article: A loss of smell can be one of the earliest warning signs of Alzheimer’s disease, but the reasons behind this sensory change have been unclear. Now, a study reveals that the problem may not lie in the nose or olfactory bulb itself, as previously thought.

[Researchers](https://www.nature.com/articles/s41467-025-62500-8) At Germany’s DZNE and Ludwig-Maximilians-Universität München (LMU) set out to investigate just why olfactory deficits (the loss of smell) often appear early in Alzheimer’s disease (AD), long before memory loss or other symptoms. They focused on the locus coeruleus (LC), a lesser studied region of the brain.

„The locus coeruleus regulates a variety of physiological mechanisms,“ explained Dr. Lars Paeger, a scientist at DZNE and LMU. „These include, for example, cerebral blood flow, sleep-wake cycles, and sensory processing. The latter applies, in particular, also to the sense of smell.“

Using a mouse model that mirrored early signs of AD-like pathology in the human brain, researchers homed in on the LC – a small region that sends out long projections (axons) to key areas across the brain, including the olfactory bulb, where smells are first processed. These axons don’t carry smell signals themselves; instead they release noradrenaline, a neurotransmitter that plays a key role in sensory tuning, attention and arousal.

The animals‘ brains had early-onset AD signs like amyloid-beta buildup and neuronal hyperactivity, but had not yet experienced widespread cell death – a hallmark of the disease as it progresses.