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▎The editor of WuXi AppTec's content team recently published a preclinical study in the top academic journal Nature, which opened the door to new treatments for patients with advanced Parkinson's disease
.
Image source: 123RF Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease, affecting the health of millions of people
.
Studies in the past few decades have pointed out that in the brains of patients with Parkinson’s disease, dopamine-releasing neurons are constantly lost, leading to the destruction of the motor function regulated by these nerve cells, resulting in slowness, stiffness, uncontrollable tremor and other movement disorders Symptoms
.
Levodopa (levodopa) is currently a commonly used drug to replace dopamine to help patients with Parkinson's disease reduce symptoms
.
However, over time, levodopa becomes less effective, making the treatment of patients with advanced Parkinson's disease extremely difficult
.
In this new study, researchers from Northwestern University in the United States revealed a new mechanism of Parkinson’s disease causing movement disorders, and designed a gene therapy based on the discovery of the new mechanism, which helps to increase the effect of levodopa on Efficacy of advanced Parkinson's disease
.
In previous studies, people discovered a small area of the brain called substantia nigra, where dopamine-releasing neurons are the first neurons to be damaged in Parkinson's disease
.
In these neurons, the researchers also noticed the characteristic of mitochondrial damage
.
Mitochondria are equivalent to the power plant of the cell and are a vital organelle for energy production
.
However, whether mitochondrial damage is the cause or result of Parkinson's disease has long been controversial
.
In the opinion of neuroscientist Professor James Surmeier, clarifying this problem is very important for the development of effective therapies
.
If it is proved that mitochondrial damage is the cause of the disease, then trying to maintain the function of mitochondria is expected to slow or prevent the progression of Parkinson's disease
.
▲Mitochondria are an important "power plant" for cells to produce energy (picture source: 123RF) In order to answer the above controversy, Professor Surmeier's research team used advanced genetic tools to construct a new genetically engineered mouse that interferes with dopaminergic The function of mitochondrial complex I in neurons causes problems in the mitochondrial metabolism of these neurons
.
Due to the shutdown of the "power plant", these cells lack sufficient energy and will eventually become exhausted and die
.
However, the researchers found that after the mitochondria were damaged, these neurons unexpectedly remained intact for a relatively long period of time
.
Initially, these neurons extend to the axons of the striatum in the adjacent brain area to reduce dopamine release
.
The loss of dopamine in the striatum has always been considered the only cause of dyskinesia in Parkinson’s disease.
However, experiments have shown that only after the striatum reduces dopamine, the mice will suffer from fine motor disorders, but they are not enough to develop Parkinson’s disease.
Related motor deficits
.
Researchers have observed that these neurons in mice actually release dopamine in the substantia nigra through cell bodies and dendrites to maintain specific motor functions
.
Until a few months later, nerve cells release less and less dopamine to the substantia nigra.
Eventually, the axons degenerate and the cells slowly die
.
At the same time, these mice showed dyskinesias typical of human advanced Parkinson's disease
.
▲ Mitochondrial damage caused the neurons in the substantia nigra to gradually reduce the release of dopamine (picture source: reference [2]) Based on the above experimental results, the researchers summarized two important findings: mitochondrial damage is sufficient to cause Parkinson's disease Development and the loss of the function of releasing dopamine in the substantia nigra is the key to the occurrence of dyskinesia
.
These new discoveries provide scientists with a new therapeutic goal: supplement dopamine in the substantia nigra
.
The researchers designed a gene therapy that targets the substantia nigra so that the cells there can convert levodopa into available dopamine
.
A proof-of-concept experiment carried out in mice shows that this therapy effectively improves the therapeutic effect of levodopa in the advanced stage of Parkinson's disease
.
Professor Surmeier commented that they hope that a new model of Parkinson’s disease based on mitochondrial disorders can help them develop new detection methods, diagnose patients with Parkinson’s disease 5 to 10 years in advance, so as to start treatment as soon as possible, and ultimately help patients change the disease.
Progress
.
Reference: [1] Patricia González-Rodríguez et al.
, (2021) Disruption of mitochondrial complex I induces progressive parkinsonism.
Nature Doi: https://doi.
org/10.
1038/s41586-021-04059-0[2] Zak Doric (2021) Mice with disrupted mitochondria used to model Parkinson's disease Nature Doi: https://doi.
org/10.
1038/d41586-021-02955-z[3] Gene therapy boosts Parkinson's disease drug benefits.
Retrieved Nov.
4, 2021 from https://news.
feinberg.
northwestern.
edu/2021/11/gene-therapy-boosts-parkinsons-disease-drug-benefits/
.
Image source: 123RF Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease, affecting the health of millions of people
.
Studies in the past few decades have pointed out that in the brains of patients with Parkinson’s disease, dopamine-releasing neurons are constantly lost, leading to the destruction of the motor function regulated by these nerve cells, resulting in slowness, stiffness, uncontrollable tremor and other movement disorders Symptoms
.
Levodopa (levodopa) is currently a commonly used drug to replace dopamine to help patients with Parkinson's disease reduce symptoms
.
However, over time, levodopa becomes less effective, making the treatment of patients with advanced Parkinson's disease extremely difficult
.
In this new study, researchers from Northwestern University in the United States revealed a new mechanism of Parkinson’s disease causing movement disorders, and designed a gene therapy based on the discovery of the new mechanism, which helps to increase the effect of levodopa on Efficacy of advanced Parkinson's disease
.
In previous studies, people discovered a small area of the brain called substantia nigra, where dopamine-releasing neurons are the first neurons to be damaged in Parkinson's disease
.
In these neurons, the researchers also noticed the characteristic of mitochondrial damage
.
Mitochondria are equivalent to the power plant of the cell and are a vital organelle for energy production
.
However, whether mitochondrial damage is the cause or result of Parkinson's disease has long been controversial
.
In the opinion of neuroscientist Professor James Surmeier, clarifying this problem is very important for the development of effective therapies
.
If it is proved that mitochondrial damage is the cause of the disease, then trying to maintain the function of mitochondria is expected to slow or prevent the progression of Parkinson's disease
.
▲Mitochondria are an important "power plant" for cells to produce energy (picture source: 123RF) In order to answer the above controversy, Professor Surmeier's research team used advanced genetic tools to construct a new genetically engineered mouse that interferes with dopaminergic The function of mitochondrial complex I in neurons causes problems in the mitochondrial metabolism of these neurons
.
Due to the shutdown of the "power plant", these cells lack sufficient energy and will eventually become exhausted and die
.
However, the researchers found that after the mitochondria were damaged, these neurons unexpectedly remained intact for a relatively long period of time
.
Initially, these neurons extend to the axons of the striatum in the adjacent brain area to reduce dopamine release
.
The loss of dopamine in the striatum has always been considered the only cause of dyskinesia in Parkinson’s disease.
However, experiments have shown that only after the striatum reduces dopamine, the mice will suffer from fine motor disorders, but they are not enough to develop Parkinson’s disease.
Related motor deficits
.
Researchers have observed that these neurons in mice actually release dopamine in the substantia nigra through cell bodies and dendrites to maintain specific motor functions
.
Until a few months later, nerve cells release less and less dopamine to the substantia nigra.
Eventually, the axons degenerate and the cells slowly die
.
At the same time, these mice showed dyskinesias typical of human advanced Parkinson's disease
.
▲ Mitochondrial damage caused the neurons in the substantia nigra to gradually reduce the release of dopamine (picture source: reference [2]) Based on the above experimental results, the researchers summarized two important findings: mitochondrial damage is sufficient to cause Parkinson's disease Development and the loss of the function of releasing dopamine in the substantia nigra is the key to the occurrence of dyskinesia
.
These new discoveries provide scientists with a new therapeutic goal: supplement dopamine in the substantia nigra
.
The researchers designed a gene therapy that targets the substantia nigra so that the cells there can convert levodopa into available dopamine
.
A proof-of-concept experiment carried out in mice shows that this therapy effectively improves the therapeutic effect of levodopa in the advanced stage of Parkinson's disease
.
Professor Surmeier commented that they hope that a new model of Parkinson’s disease based on mitochondrial disorders can help them develop new detection methods, diagnose patients with Parkinson’s disease 5 to 10 years in advance, so as to start treatment as soon as possible, and ultimately help patients change the disease.
Progress
.
Reference: [1] Patricia González-Rodríguez et al.
, (2021) Disruption of mitochondrial complex I induces progressive parkinsonism.
Nature Doi: https://doi.
org/10.
1038/s41586-021-04059-0[2] Zak Doric (2021) Mice with disrupted mitochondria used to model Parkinson's disease Nature Doi: https://doi.
org/10.
1038/d41586-021-02955-z[3] Gene therapy boosts Parkinson's disease drug benefits.
Retrieved Nov.
4, 2021 from https://news.
feinberg.
northwestern.
edu/2021/11/gene-therapy-boosts-parkinsons-disease-drug-benefits/
