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Overactive neurons in specific regions of the brain are thought to be early disturbances of Alzheimer's disease. In a new study, researchers from the Technical University of Munich, Germany, were the first to explain the causes and mechanisms of this early important neurological dysfunction. They found that the excitatory neurotransmitter glutamate persisted for too long in the vicinity of active neurons. This causes these neurons to suffer from pathological over-stimulation, which is likely to be a key factor in learning and memory loss in patients with Alzheimer's disease. The results of the study were published in the August 9th, 2019 issue of Science, entitled 'A vicious cycle of β amyloid–dependent neuronal hyperactivation.'
The brains of patients with Alzheimer's disease who have developed clinical symptoms contain large β-amyloid masses (ie, plaques). Many treatments focus on the removal of plaques, but so far this attempt has only met with limited success.
Arthur Konnerth, author of the paper and professor of neuroscience at the Technical University of Munich, explains, “We are critical to detecting and treating this disease earlier. Therefore, we focus on overactive neurons, which are more common in this disease. It occurs early, and it occurs long before the patient has memory loss.' Because of hyperactivity, neurons connected together in the neural circuit constantly receive false signals, which leads to damage to signal processing.
Konnerth, his PhD student Benedikt Zott, and his team succeeded in identifying the causes and triggers that triggered this early disturbance in the brain. This discovery may open the way for new treatments.
Neurons communicate with each other using chemicals called neurotransmitters. As one of the most important chemicals, glutamate plays a role in activating neurons that are connected together. Glutamate is released at a junction site called a synapse between two neurons and is quickly removed to allow propagation of the next signal. This removal involves the so-called active pump molecules and the passive transport of glutamate along nearby cell membranes.
These researchers found that high concentrations of glutamate persisted for too long in the synaptic cleft of highly active neurons. This is due to the action of beta-amyloid molecules: they prevent glutamate from transporting out of the synaptic cleft. They tested this mechanism using beta-amyloid molecules from patient samples and tested them using various mouse models, all with similar results.
he researchers also found that this neurotransmitter blockade is mediated by early soluble beta-amyloid rather than plaque. Beta-amyloid is initially present in a single molecule form (monomer) and then aggregates into a bimolecular form (dimer) and a larger β-amyloid chain, eventually forming plaques. They found that glutamate blockade is caused by soluble beta-amyloid dimers.
As the first author of the paper, Benedict Zott, outlined, “Our data provide clear evidence for the rapid and direct toxic effects of a specific β-amyloid (ie, dimer). We can even explain this. mechanism.' These researchers now want to use this knowledge to further enhance their understanding of the cellular mechanisms of Alzheimer's disease and support the development of treatment strategies for the early stages of the disease.
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