New Cause of Parkinson’s Disease Found
Prof. Daesoo Kim’s team traces disease to excitatory motor signals
A study led by Prof. Daesoo
Kim of KAIST has overturned 30 years of consensus on the cause of Parkinson’s disease.
The team showed that
inhibitory basal ganglia inputs excite target neurons instead of suppressing
them, leading to motor dysfunction in Parkinson’s disease.
Parkinson’s disease is caused by insufficient levels of
dopamine in the brain; its symptoms include rigid muscles, slowed movement, and
trouble walking. There is currently no cure for the disease.
Most treatments for Parkinson’s rely on motor signal suppression theory,
proposed by Dr. Delong’s team in the 1980s. According
to this theory, inhibitory basal ganglia inputs interfere with motor function
by suppressing motor neurons.
The basal ganglia secrete GABA
in the thalamus; the amount of secretion increases under low levels of
dopamine, which are a feature of Parkinson’s disease. However, this theory has limitations in explaining the
disease’s complex symptoms.
The team employed optogenetics
to stimulate inhibitory basal ganglia inputs in mice, so as to induce symptoms
similar to those of patients suffering from Parkinson’s disease. The ventrolateral thalamic neurons appeared to be
temporarily suppressed, but were in fact engaged in rebound firing.
The team found that mice suffering
from Parkinson’s disease completely recovered
when rebound firing was inhibited. They explained that inhibitory basal ganglia
inputs induce excitatory motor signals instead of motor suppression.
Prof. Kim said, "Symptoms
of Parkinson’s disease can be suppressed by
inhibiting rebound firing. This finding will lead to the development of new
treatments for Parkinson’s patients with low levels of
Funded by the Ministry of
Science and ICT and the National Research Foundation of Korea, the study was
published in the prestigious Neuron on August 30.
Parkinson’s symptoms caused by
inhibitory basal ganglia inputs
Success in recovering from Parkinson’s
based on optogenetics
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