Researchers at the Institut Pasteur reveal how a brain receptor called nicotinic α7 plays a central role in neuronal communication disorders at the onset of Alzheimer's disease. This breakthrough paves the way for new targeted therapies to slow the onset of dementia.
Alzheimer's disease affects nearly 1.4 million people in France and remains one of the most feared diseases of old age. Among its first signs: disruption of communication between neurons, well before the massive loss of brain cells. To understand this phenomenon, the Integrative Neurobiology of Cholinergic Systems unit, led by Uwe Maskos at the Institut Pasteur, examined a key player: the α7-type nicotinic receptor, an essential gateway for chemical signals in the brain.
Using an animal model, the researchers showed that the accumulation of a small fragment, beta-amyloid (a classic marker of Alzheimer's), causes abnormal hyperactivity of neurons, but only if the α7 receptor is present. Removing this receptor prevents the dysfunction; reintroducing it brings the problem back. This mechanism explains why certain drugs already in use, such as galantamine, appear to offer better protection: they specifically target this receptor and reduce hyperactivity. A recent large Swedish study confirms that galantamine slows memory loss in many patients (source). By analyzing clinical data from a large cohort of Swedish patients (The SveDem quality registry), "we show that if galantamine has a greater effect against dementia—and death—it's because this molecule acts on the nicotinic receptor," emphasizes Uwe Maskos. "We establish the action of galantamine and describe the underlying mechanism on the nicotinic receptor."
This research highlights the nicotinic receptor as a new priority target for treating the early stages of Alzheimer's disease and offers new avenues for developing more effective treatments. Better understanding and protecting our "neuronal connection" could help delay the first symptoms of a disease that affects more and more families.
** This text was translated using an AI-powered translation tool **
Source :
The alpha7 nicotinic acetylcholine receptor mediates network dysfunction in a mouse model of local amyloid pathology, Molecular Psychiatry, 23 septembre 2025.
Fani Koukouli, Chun-Lei Zhang, Ivan Lazarevich, et al.
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