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▎Edited by WuXi AppTec's content team Autism, schizophrenia and other neurodevelopmental disorders have complex genetic factors, and patients also have a series of different symptoms
.
However, researchers have noticed that some symptoms are common in a variety of neurodevelopmental disorders, such as learning disabilities and attention deficits
.
Researchers at the Massachusetts Institute of Technology (MIT) recently discovered that although the factors that cause disease may vary from person to person, cognitive impairment may have the same neural mechanism behind it
.
This research was published today in Neuron, an authoritative academic journal in the field of neuroscience
.
Researchers have revealed through mouse studies that some genes that are mutated or missing in patients with autism or schizophrenia cause similar neural circuit dysfunctions in the thalamus "by different routes"
.
This means that as long as drugs can be developed to repair this loop, it is expected to treat many different mental disorders
.
Professor Feng Guoping, who led this research, pointed out: “This research reveals a new loop mechanism for cognitive impairment, and points out the future direction of the development of new therapies-not based on the comprehensive behavior shown by the patient, but based on the underlying behavior.
The neurobiological mechanism of the brain is used to classify different patients
.
” ▲Professor Feng Guoping (photo source: McGovern Brain Research Institute) Recent studies have shown that the thalamus, located deep in the brain, is not only involved in sensory information transmission, but also in learning and memory.
It also plays a certain role in the formation process
.
Scientific research has found that some genes related to cognitive impairment are often highly expressed in this brain area
.
In particular, many autism and schizophrenia risk genes are expressed in the anterodorsal thalamus (AD)
.
The team led by Professor Feng Guoping conducted long-term research on the autism risk gene Ptchd1
.
When they used CRISPR-Cas9 technology to inhibit the expression of the Ptchd1 gene in mouse thalamus AD, they observed that the animals had memory impairment
.
Using novel technology to track the neural projections of thalamic AD, the researchers found that the AD area of the thalamus is connected to another area of the brain called the retrosplenial cortex (RSC), and confirmed that this loop is necessary for encoding memory.
Indispensable
.
When the Ptchd1 gene is missing, this loop is disrupted, and the mouse can't remember having received an electric shock in a room, indicating that there is a problem with its spatial fear memory
.
▲ Neurons from the anterior dorsal nucleus of the thalamus (red) reveal the unique triangular structure of this subdivision in the anterior thalamic complex
.
The green is the adjacent thalamic reticular nucleus neurons, and the blue is the DAPI staining of the nucleus in this area (Image source: Reference [1]; Image credit: Dheeraj Roy and Ying Zhang) The researchers also found in this study that the thalamus The other part called the anterior ventral side (AV for short) is also involved in memory formation
.
What's interesting is that, unlike the adjacent AD area, the neural connection from AV to RSC regulates the specificity of memory, that is, it allows us to distinguish a memory segment from memory segments of similar characteristics
.
Co-first author Dr.
Dheeraj Roy said: "These experiments show that the two adjacent parts of the thalamus have different contributions to memory formation
.
This is beyond our expectations.
.
"Not only Ptchd1, the researchers conducted the same experiment on another gene related to autism and three genes related to schizophrenia, and saw similar results in all mice: reducing the expression of these genes.
Later, it will cause memory impairment
.
▲The diagram of this study (picture source: Reference [1]) More importantly, the reduction of expression of these genes will cause the neurons in the AD area of the thalamus to be overexcited
.
Researchers believe that these the results may explain why patients have memory impairment when these types of gene mutations or deletions
.
mainstream theory of learning and memory of the view that the synapse (ie, neural connections) generated during the learning process is the formation of memories is enhanced
.
"when animals When learning, these neurons must strengthen their firing activities, and the degree of strengthening is related to the degree of learning
.
A simple explanation is that if the neuron has been over-excited in the baseline state, it may not be able to further increase activity through learning
.
"Co-first author Dr.
Ying Zhang explained
.
▲This research is expected to bring about a new method of treating a variety of mental disorders (picture source: 123RF) Based on this mechanism, researchers have verified a strategy for restoring cognition through experiments
.
They Managed to artificially reduce the hyperexcitability of AD neurons in the thalamus, allowing several genetically mutant mice to regain normal cognitive functions
.
Although the chemical genetic method used in the experiment has not been approved for use in humans, the researchers That said, there are other possible ways to target this neural circuit
.
"There are many genetic and environmental factors that may cause specific diseases, but in the final analysis, these factors must cause certain types of neuronal changes and affect related neural circuits.
Specific behavior
.
"Professor Feng Guoping said, "From a therapeutic point of view, in this case, we may not track single molecules, because they may vary from person to person and are only related to a small number of patients; however, At the cell level or loop level, patients have more common characteristics
.
"Reference: [1] Dheeraj Roy et al.
, (2021) Anterior Thalamic Dysfunction Underlies Cognitive Deficits in a Subset of Neuropsychiatric Disease Models.
Neuron Doi: [2] Some brain disorders exhibit similar circuit malfunctions, Retrieved June 30, 2021, from https://news.
mit.
edu/2021/circuit-brain-disorders-0630
.
However, researchers have noticed that some symptoms are common in a variety of neurodevelopmental disorders, such as learning disabilities and attention deficits
.
Researchers at the Massachusetts Institute of Technology (MIT) recently discovered that although the factors that cause disease may vary from person to person, cognitive impairment may have the same neural mechanism behind it
.
This research was published today in Neuron, an authoritative academic journal in the field of neuroscience
.
Researchers have revealed through mouse studies that some genes that are mutated or missing in patients with autism or schizophrenia cause similar neural circuit dysfunctions in the thalamus "by different routes"
.
This means that as long as drugs can be developed to repair this loop, it is expected to treat many different mental disorders
.
Professor Feng Guoping, who led this research, pointed out: “This research reveals a new loop mechanism for cognitive impairment, and points out the future direction of the development of new therapies-not based on the comprehensive behavior shown by the patient, but based on the underlying behavior.
The neurobiological mechanism of the brain is used to classify different patients
.
” ▲Professor Feng Guoping (photo source: McGovern Brain Research Institute) Recent studies have shown that the thalamus, located deep in the brain, is not only involved in sensory information transmission, but also in learning and memory.
It also plays a certain role in the formation process
.
Scientific research has found that some genes related to cognitive impairment are often highly expressed in this brain area
.
In particular, many autism and schizophrenia risk genes are expressed in the anterodorsal thalamus (AD)
.
The team led by Professor Feng Guoping conducted long-term research on the autism risk gene Ptchd1
.
When they used CRISPR-Cas9 technology to inhibit the expression of the Ptchd1 gene in mouse thalamus AD, they observed that the animals had memory impairment
.
Using novel technology to track the neural projections of thalamic AD, the researchers found that the AD area of the thalamus is connected to another area of the brain called the retrosplenial cortex (RSC), and confirmed that this loop is necessary for encoding memory.
Indispensable
.
When the Ptchd1 gene is missing, this loop is disrupted, and the mouse can't remember having received an electric shock in a room, indicating that there is a problem with its spatial fear memory
.
▲ Neurons from the anterior dorsal nucleus of the thalamus (red) reveal the unique triangular structure of this subdivision in the anterior thalamic complex
.
The green is the adjacent thalamic reticular nucleus neurons, and the blue is the DAPI staining of the nucleus in this area (Image source: Reference [1]; Image credit: Dheeraj Roy and Ying Zhang) The researchers also found in this study that the thalamus The other part called the anterior ventral side (AV for short) is also involved in memory formation
.
What's interesting is that, unlike the adjacent AD area, the neural connection from AV to RSC regulates the specificity of memory, that is, it allows us to distinguish a memory segment from memory segments of similar characteristics
.
Co-first author Dr.
Dheeraj Roy said: "These experiments show that the two adjacent parts of the thalamus have different contributions to memory formation
.
This is beyond our expectations.
.
"Not only Ptchd1, the researchers conducted the same experiment on another gene related to autism and three genes related to schizophrenia, and saw similar results in all mice: reducing the expression of these genes.
Later, it will cause memory impairment
.
▲The diagram of this study (picture source: Reference [1]) More importantly, the reduction of expression of these genes will cause the neurons in the AD area of the thalamus to be overexcited
.
Researchers believe that these the results may explain why patients have memory impairment when these types of gene mutations or deletions
.
mainstream theory of learning and memory of the view that the synapse (ie, neural connections) generated during the learning process is the formation of memories is enhanced
.
"when animals When learning, these neurons must strengthen their firing activities, and the degree of strengthening is related to the degree of learning
.
A simple explanation is that if the neuron has been over-excited in the baseline state, it may not be able to further increase activity through learning
.
"Co-first author Dr.
Ying Zhang explained
.
▲This research is expected to bring about a new method of treating a variety of mental disorders (picture source: 123RF) Based on this mechanism, researchers have verified a strategy for restoring cognition through experiments
.
They Managed to artificially reduce the hyperexcitability of AD neurons in the thalamus, allowing several genetically mutant mice to regain normal cognitive functions
.
Although the chemical genetic method used in the experiment has not been approved for use in humans, the researchers That said, there are other possible ways to target this neural circuit
.
"There are many genetic and environmental factors that may cause specific diseases, but in the final analysis, these factors must cause certain types of neuronal changes and affect related neural circuits.
Specific behavior
.
"Professor Feng Guoping said, "From a therapeutic point of view, in this case, we may not track single molecules, because they may vary from person to person and are only related to a small number of patients; however, At the cell level or loop level, patients have more common characteristics
.
"Reference: [1] Dheeraj Roy et al.
, (2021) Anterior Thalamic Dysfunction Underlies Cognitive Deficits in a Subset of Neuropsychiatric Disease Models.
Neuron Doi: [2] Some brain disorders exhibit similar circuit malfunctions, Retrieved June 30, 2021, from https://news.
mit.
edu/2021/circuit-brain-disorders-0630
