University of Pittsburgh Professor Pascoal’s research team
[오피니언뉴스=이상석 기자] A research result has been discovered that can answer the question that many people with aggregated beta-amyloid, an abnormal protein in brain neurons, identified as the main culprit of Alzheimer’s disease, do not actually show symptoms of dementia.
A research team led by Professor Trike Paskoal, a neuropsychiatrist at the University of Pittsburgh Medical School, announced on the 30th (local time) that astrocytes, which are auxiliary cells that help brain neurons, are the key to the development of dementia.
Alzheimer’s disease is known to occur when beta amyloid, a surface protein in the space between nerve cells, and tau protein in nerve cells are misfolded and aggregate or bind together, turning into toxic proteins that kills nerve cells.
Astrocytes are star-shaped support cells that help nerve cells in the brain, make energy necessary for the brain, regulate iron and hydrogen ion concentrations, and are involved in the formation of synapses, which are signal transmission pathways in nerve cells . In a word, it can be said that the cells are in charge of keeping the house of the brain.
The research team revealed that this was the result of analyzing data from 1016 elderly people (average age 69.6) with normal cognitive functioning who took part in three related studies.
The research team measured the level of glial fibrillary acidic protein (GFAP), an indicator of activity produced by the response of astrocytes, in their blood samples. GFAP plays an important role in regulating the motility and maintaining the shape of astrocytes.
As a result, it was found that only those who showed positive reactions of beta amyloid and astrocytes also had tawoopathy.
The research team explained that this suggests that beta amyloid and astrocyte reaction positivity could be signs that predict clinical symptoms of dementia.
Tauopathy refers to neurodegenerative diseases caused by abnormal structure formation through misfolding of the tau protein.
Representative diseases include Alzheimer’s disease, Parkinson’s disease, Lewy body dementia, Down syndrome, and progressive supranuclear palsy (PSP).
In previous studies, the research team found that increased inflammation in the brain, as much as beta amyloid aggregation, triggers a pathological chain reaction called the death of brain neurons.
Inflammation in brain tissue spreads pathologically misfolded proteins in brain neurons, which is a direct cause of impaired cognitive function in dementia patients.
The research team explained that astrocytes regulate the relationship between beta amyloid and tau like an orchestra conductor.
The research team expected that this result could be used in clinical trials of dementia treatment candidates in the future.
Because many people with abnormal beta-amyloid do not develop clinical symptoms of dementia, having beta-amyloid alone is not enough to be eligible to participate in clinical trials to confirm the effectiveness of dementia treatment candidates.
The research team pointed out that adding an astrocyte response marker such as GFAP to this will allow an accurate selection of clinical trial participants who will show symptoms of dementia in the future.
The results of this study were published in the latest issue of Nature Medicine, a British medical journal.
Reporter Lee Sangemail@example.com
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