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The cause of Alzheimer’s dementia patients unable to smell: Dong-A Science

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DGIST-Maastricht University, Netherlands joint research

DGIST Brain and Cognitive Science Professor Moon Il Moon, Dr. Son Go-woon, and Professor Zaanshahi of Maastricht University in the Netherlands (from left) participated in this study. Provided by DGIST.

A Korean research team has identified the cause of loss of smell in Alzheimer’s patients. It is expected to help develop a diagnostic method or treatment for Alzheimer’s disease.

The Daegu Gyeongbuk Institute of Science and Technology (DGIST) announced on the 22nd that a research team led by Professor Il Moon of the Department of Brain and Cognitive Sciences and researchers from Maastricht University in the Netherlands discovered the cause of the loss of smell in Alzheimer’s dementia patients from the olfactory tissue of a post-mortem donor. said.

According to data from the Ministry of Health and Welfare, the number of dementia patients in 2017 was about 700,000, and it is expected to increase to 3.03 million by 2050. Alzheimer’s disease accounts for 70% of all dementia patients. Most Alzheimer’s patients suffer from memory and cognitive decline, as well as depression and sensory dysfunction. In more than 90% of cases, the sense of smell is lost, and the pathological cause has not yet been identified.

In order to maintain the normal olfactory function, the olfactory glomeruli present in the olfactory bulb, which first information olfactory signals, must be structurally and functionally free. The olfactory bulb is an elongated bulge below the frontal lobe of the cerebral cortex and refers to the part containing the olfactory nerve. The area where the olfactory cells and nerve fibers connect in the olfactory bulb is called the olfactory glomerulus. The research team intensively studied the structure and function of the olfactory glomerulus in Alzheimer’s patients to identify the cause of the loss of smell due to Alzheimer’s dementia.

The research team received olfactory bulb tissues from 6 Alzheimer’s dementia patients and 7 healthy donors donated post-mortem from the Dutch Brain Bank and observed changes in the structure of the olfactory glomerulus. Immunochemical analysis was used to analyze changes in the overall anatomy and histology, as well as changes in the expression of ‘beta-amyloid’ protein, known as the cause of Alzheimer’s, ‘microglia’, the most distributed cell in the brain, and neurotransmitters.

As a result of the analysis, morphological damage in which the olfactory bulb atrophy was observed in Alzheimer’s dementia patients. Accumulation of beta-amyloid protein was observed in the olfactory glomerulus, and the expression level of neurotransmitters related to synaptic activity was decreased. It was also confirmed that synapses in the olfactory glomerulus were atrophied.

In particular, the researchers found that beta-amyloid accumulation was also associated with microglia activity. This means that olfactory glomerular abnormalities due to neuroinflammation can directly affect the loss of smell in Alzheimer’s dementia patients. This is the first evidence of a relationship between beta-amyloid-induced neuroinflammation and loss of smell in Alzheimer’s patients.

Professor DGIST, who is the problematic, said, “It is very meaningful that we eventually found that damage to the olfactory glomeruli, which forms a synapse between the peripheral olfactory nervous system and the central olfactory nervous system, is important in the development of Alzheimer’s dementia.” The results of this study were published online on the 28th of October in the international scientific journal ‘Brain Pathology’.


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