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Korean researchers successfully identified the source of memory impairment in a brain plagued by Alzheimer’s disease, the Ministry of Science, ICT and Future Planning said Monday.
By pinpointing the potential target for treatment, the discovery is expected to open up the possibility of developing new drugs for the illness, which is considered the most common form of dementia.
The key to the impairment lies in the reactive astrocytes that build up after the brain is affected by the disease, according to the researchers from the Korea Institute of Science and Technology.
They found that reactive astrocytes in affected mice started producing abnormally large amounts of the inhibitory neurotransmitter gamma-Aminobutyric acid, or GABA. This happens via a reaction with oxidase-B, or Mao-B, an enzyme believed to be associated with both Alzheimer’s disease and Parkinson’s disease.
GABA is then released through the anion channel of Bestrophin-1 and acts on presynaptic GABA receptors, hindering the normal signal transmission of nerve cells.
By suppressing the GABA production or release from reactive astrocytes, the researchers were able to fully restore the impaired learning and memory along with other abnormalities that occurred to the mice with the increasing GABA.
A postmortem study of the affected mice showed that the level of astrocytic GABA and Mao-B were both significantly upregulated in the brain.
“The study showed that repressing the production of GABA by the reactive astrocytes and its release could be a new cure to restore memory loss from Alzheimer’s disease,” said lead researcher Lee Chang-jun, a scientist from the Brain Science Institute at the KIST. “We managed to establish a foundation to develop a treatment which effects persist, even upon long-term use.”
Scientists around the world have attempted to find a cure for Alzheimer’s disease since it was first observed in 1906, but to no avail. In 2013, some 580,000 people were reported to be suffering from dementia, and Alzheimer’s disease accounted for 71 percent of them.
By Yoon Min-sik (minsikyoon@heraldcorp.com)
By pinpointing the potential target for treatment, the discovery is expected to open up the possibility of developing new drugs for the illness, which is considered the most common form of dementia.
The key to the impairment lies in the reactive astrocytes that build up after the brain is affected by the disease, according to the researchers from the Korea Institute of Science and Technology.
They found that reactive astrocytes in affected mice started producing abnormally large amounts of the inhibitory neurotransmitter gamma-Aminobutyric acid, or GABA. This happens via a reaction with oxidase-B, or Mao-B, an enzyme believed to be associated with both Alzheimer’s disease and Parkinson’s disease.
GABA is then released through the anion channel of Bestrophin-1 and acts on presynaptic GABA receptors, hindering the normal signal transmission of nerve cells.
By suppressing the GABA production or release from reactive astrocytes, the researchers were able to fully restore the impaired learning and memory along with other abnormalities that occurred to the mice with the increasing GABA.
A postmortem study of the affected mice showed that the level of astrocytic GABA and Mao-B were both significantly upregulated in the brain.
“The study showed that repressing the production of GABA by the reactive astrocytes and its release could be a new cure to restore memory loss from Alzheimer’s disease,” said lead researcher Lee Chang-jun, a scientist from the Brain Science Institute at the KIST. “We managed to establish a foundation to develop a treatment which effects persist, even upon long-term use.”
Scientists around the world have attempted to find a cure for Alzheimer’s disease since it was first observed in 1906, but to no avail. In 2013, some 580,000 people were reported to be suffering from dementia, and Alzheimer’s disease accounted for 71 percent of them.
By Yoon Min-sik (minsikyoon@heraldcorp.com)
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