Researchers Gye-ju Lee and Yu-na Jang “Abnormal expression of specific proteins causes synaptic damage”
Researcher Gye-ju Lee and researcher Yu-na Jang (front) confirm protein expression. Provided by Korea Brain Research Institute
A research team at the Korea Brain Research Institute identified the mechanism that causes Alzheimer’s disease and published it in an international journal.
According to the Brain Research Institute on the 18th, the neurological circuit research group, including senior researcher Gye-ju Lee (corresponding author) and researcher Yu-na Jang (first author), identified that excessive expression of the protein’RAPGEF2′ is a mechanism that causes Alzheimer’s disease synaptic damage. RAPGEF2 is a protein that plays an important role in neuronal development in neurons.
Alzheimer’s disease is the most common degenerative brain disease that accounts for 75% of dementia. It is a terrifying disease that causes memory loss, manic depression, and speech impairment as time passes, but there is no cure to completely stop Alzheimer’s disease symptoms.
However, it is suggested as a representative hypothesis that abnormal aggregation of amyloid beta (Aβ) and tau protein is the cause of the disease. Amyloid beta is known to cause cognitive impairment by damaging the synapse, which is a memory storage location in the brain.
Accordingly, the research team discovered that amyloid beta promotes the overexpression of RAPGEF2 protein, resulting in loss of synapses through various neurobiological studies. In other words, suppressing RAPGEF2 expression can prevent synapse reduction and cognitive impairment.
The results of this study are meaningful in that the molecular mechanism of synaptic damage that appears in the early stages of Alzheimer’s disease has been specifically identified.
Principal Researcher Lee Gye-ju said, “I hope this study will be used as an important source data for understanding the specific mechanisms of synaptic-damaging brain diseases such as Alzheimer’s disease and developing new treatment strategies.”
The paper containing the research results was listed in the January 2021 issue of the online edition of the British Journal of Neuropathology, the top 10% in clinical neuroscience and the top 5% in pathology.