Researchers from the Karolinska Institute, in collaboration with Japanese counterparts, have determined that modulating specific receptors within the brain can hasten the breakdown of beta-amyloid (Aβ)—the protein responsible for forming hazardous plaques characteristic of Alzheimer’s disease. These findings have been featured in the JAD (Journal of Alzheimer’s Disease).
The scientific team evaluated an experimental compound designed to stimulate the somatostatin receptors known as SST1 and SST4. These receptors play a role in controlling the levels of neprilysin, an enzyme critical for dismantling Aβ within the hippocampus, a brain region vital for both memory and spatial awareness.
During trials conducted on mice exhibiting symptoms mimicking Alzheimer’s pathology, the scientists achieved notable outcomes: administering the compound resulted in elevated concentrations of neprilysin in the animals’ brains, a reduction in beta-amyloid accumulation, and discernible improvements in their cognitive capabilities. Importantly, no significant adverse effects were observed.
Of particular significance is the perspective held by the researchers that medications targeting SST1 and SST4 could potentially be manufactured efficiently and formulated into a convenient pill format. This advancement would substantially streamline their prospective utilization in clinical settings.
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