2023-06-09 00:00:00
Alzheimer’s disease affects approximately one million people in France. It is a heterogeneous disease as to its origin, its clinical evolution or its lesions. Today, the factors modulating the clinical evolution of the pathology are still poorly understood.
The disease is linked to the presence of deposits of amyloid-β (Aβ) proteins which lead to a cascade of events leading to a loss of synapses (thereby limiting the ability of neurons to communicate with each other) and ultimately to alterations in memory.
Several studies have established that intracerebral administration of compounds contaminated with amyloid-β can induce amyloid-β pathology.
Some people have genetic mutations that induce the production of mutated forms of Aβ.
In this study, scientists showed that a single exposure of mouse models of amyloid pathology to certain mutated forms of Aβ can worsen Alzheimer’s disease damage as well as downstream events including cognition, connectivity brain and synapse health several months following inoculation.
Furthermore, this mutated Aβ increases the ability of native Aβ to aggregate. Of course, an event like intracerebral inoculation of mutated Aβ is not clinically relevant.
However, the study highlights that a single event regulating Aβ aggregation and synaptic health can have long-term impacts and the originality of the study is that it demonstrates a behavioral impact.
This first study showing that a single sporadic event such as the inoculation of mutated Aβ can aggravate the outcome of the pathology and the clinical evolution several months following the event is therefore important because it suggests that Aβ can initiate mechanisms that regulate a cascade of events over a long period of time.
Further studies are now needed to determine the relationships between mutated Aβ and its functional impact.
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