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Scientists have discovered that the first target of Alzheimer's disease is the sense of smell
Last reviewed: 30.06.2025

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Alzheimer's disease primarily damages olfactory neurons. Researchers from the National Institute of Neurological Disorders and Stroke in Bethesda, USA, have proven this in experiments on laboratory mice. Thus, it becomes clear why patients who develop senile dementia first lose their sense of smell.
"Difficulty in perceiving and distinguishing smells is an early symptom of Alzheimer's disease," explains Leonardo Belluscio, the study's leader. "And this symptom can serve as an early diagnostic tool for the disease. The changes that occur in the olfactory system are similar to those that occur throughout the brain, but they begin earlier."
Most experts associate the causes of Alzheimer's disease with the beta-amyloid protein, which is deposited in the neurons of the brain in the form of plaques, which leads to the degradation and death of nerve cells. New data have shown that the pathology leading to the death of neurons develops even before the appearance of plaques.
Belluscio and his colleagues worked with genetically modified mice whose olfactory neurons produced a mutant version of the human protein beta-amyloid precursor protein (APP). In humans, this mutation accompanies the early onset of Alzheimer's disease (before age 65), and early onset of the disease has been shown to be familial.
At three weeks of age, mice with the mutant APP had four times as many olfactory neurons dying as control animals. And plaques did not form in these neurons. This convinced the scientists that the neuron death was not directly related to plaques, but was related only to the mutant protein. When they reduced its high levels in the olfactory neurons, they stopped dying.
This gave the researchers hope: it meant that they had not only confirmed that the olfactory cells were taking the first hit, but had also shown that the pathological process could be stopped.