Soluble amyloid beta disrupts the function of olfactory sensory neurons prior to the onset of the amyloid plaques that are commonly associated with Alzheimer’s disease. These findings, reported in Nature Communications this week add to the growing evidence that amyloid beta proteins may be the major causal factor in initiating the disease.
Alzheimer’s disease is characterised by the presence of amyloid plaques throughout the brain. However, there is growing debate about whether the pathological changes associated with amyloid beta proteins are a cause or consequence of Alzheimer’s disease development.
Mark Albers and colleagues use two new transgenic mouse models to investigate the actions of human amyloid beta proteins on the olfactory circuit. They find that the neural network involved in olfactory perception and odour discrimination is compromised due to abnormal targeting by olfactory sensory neurons and caused by the amyloid beta proteins before they form plaques.
The authors suggest that these findings, which are applicable to various neural circuits in the brain, could lead the way in the search for new, more effective therapies that are specific for the early stages of Alzheimer’s disease before symptoms begin to appear.
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