Researchers delve deeper into the neuronal mechanisms that underlie olfactory dysfunction in Alzheimer’s

Loss of smell or olfactory dysfunction is an early symptom of Alzheimer’s neurodegenerative disease (AD) and occurs in approximately 90% of all patients. Although odor loss is a major symptom, patients with AD can only recognize specific odors and do not completely lose their odor; this suggests that the olfactive center may play a specific role in the brain.

Amyloid β (Aβ), a toxic protein that accumulates in the brain is a contributing factor in AD pathogenesis and is also present in the olfactory system that controls the sensation of smell. However, the epidemiology and mechanisms in AD-specific olfactory dysfunction involving olfactory sensory neurons (OSNs) remain unclear.

To address this gap, a group of researchers from DGIST, Korea, led by Professor Cheil Moon, conducted an in-depth study to understand the neuronal mechanisms underlying olfactory dysfunction in AD. Talking about their latest study, recently published in Alzheimer’s Research and Treatment, Dr. Moon says, “We have been particularly interested in the specific regional degeneration of sensory neurons in the olfactory system during AD progression. In our new study, we examine the link between psychology and behavior. olfactory using an AD mouse model to understand the involvement of olfactory neurons in disease pathogenesis »

In this study, the researchers used a mutant mouse model expressing high levels of Aβ and exhibiting nervous system deficiencies similar to AD pathology. They tested whether the mice were able to detect hidden food based on smell and where they could identify and differentiate several odors. They found that the mice needed a much longer time to seek food and exhibited partial olfactory disorder. They confirmed these physically using a calcium-based sensor: they found that the mice were receptive to certain odors but could not recognize others due to neuronal deficits in specific areas of the t. -olfactory system.

Interestingly, when they dug deeper, they found that the Aβ protein was unevenly distributed across different anatomical regions of the olfactory system. Moreover, the regions that expressed higher levels of Aβ were, in fact, those regions that exhibited lower activity of OSNs and lower odor detection. This clarifies the role of region-specific Aβ accumulation in olfactory dysfunction.

In addition, the researchers also identified anatomical defects and lower neuron turnover that are indicative of less proliferation and higher neuron mortality in certain olfactory regions including the olfactory epithelium and bulb tends to contribute to odor loss.

Dr. will. Moon concludes by recounting the long-term impact of their work. He says, “Partial loss of smell can be a potential diagnostic strategy for developing early screening of people at risk of AD. The findings of our study contribute to understanding of the link between AD progression and Aβ accumulation in the olfactory system that may further advance. interesting therapeutic targets will emerge. “