-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Written | Edited by Wang Cong | Nagashi Typesetting | Shui Chengwen On April 25, 1953, James Watson, Francis Crick, Rosalind Franklin, Wilkins and others simultaneously published 3 papers in Nature.
Uncovering the mystery of DNA structure for the first time, mankind officially opened the era of molecular biology.
Since then, the iconic double helix structure has become the public's default impression of DNA.
However, as the most important genetic material, is DNA only this kind of structure? In January 2013, Nature Chemistry published a paper, which showed that there is an unusual four-stranded DNA structure in human cells-G-quadruplexes.
On March 23, 2021, researchers from the University of Montreal in Canada published a research paper titled: G-quadruplexes originating from evolutionary conserved L1 elements interfere with neuronal gene expression in Alzheimer's disease in the journal Nature Communications.
The study found that inactivation of the BMI1 gene in human cells or mice can cause heterochromatin relaxation and induce the appearance of G-quadruplex structures.
In neurodegenerative diseases, heterochromatin relaxation in neurons often occurs, and G-quadruplex structures are accumulated in neurons in the brain of Alzheimer's patients.
The study discovered a new function of the BMI1 gene: to prevent the formation of a disordered G-quadruplex structure in the DNA of brain neurons, thereby preventing Alzheimer's disease and inhibiting brain aging.
This research has increased our understanding of the basic mechanisms of Alzheimer's disease, allowing us to further understand Alzheimer's disease.
Alzheimer's disease (AD), commonly known as "Alzheimer's disease", is a serious neurodegenerative disease.
Patients usually suffer from memory decline and weakened learning ability, accompanied by emotional regulation.
Obstacles and loss of athletic ability greatly affect the development of individuals, families and even society.
Currently, about 50 million people worldwide suffer from Alzheimer's disease.
As the average life expectancy of human beings increases and the aging society intensifies, the prevalence of Alzheimer's disease is also rising.
It is estimated that by 2050, Alzheimer's patients will increase to more than 150 million.
Prior to this, the research team published in the journals Cell Reports and Scientific Reports showed that the BMI1 gene has become particularly low in the brains of Alzheimer’s disease patients.
They also found that the BMI1 gene in human neurons and mouse neurons The inactivation is sufficient to generate all the pathological markers associated with Alzheimer's disease.
These findings indicate that the activity of the BMI1 gene is closely related to the onset of Alzheimer's disease, and it is likely to play a function of inhibiting Alzheimer's disease.
In this Nature Communications paper, the research team found that G-quadruplex structures accumulate in the brain neurons of Alzheimer's patients, but not in the brains of healthy elderly people.
Healthy neurons (left), Alzheimer's neurons (right): Green is the accumulation of G4 structures in Alzheimer's neurons.
This study found that inactivation of the BMI1 gene in human cells or mice can lead to heterochromatin Relax and induce the appearance of G-quadruplex structure.
In neurodegenerative diseases, heterochromatin relaxation in neurons often occurs, and G-quadruplex structures are accumulated in neurons in the brain of Alzheimer's patients.
The study discovered a new function of the BMI1 gene: to prevent the formation of a disordered G-quadruplex structure in the DNA of brain neurons, thereby preventing Alzheimer's disease and inhibiting brain aging.
So far, Alzheimer's disease is still incurable.
Therefore, any progress in this field can bring hope to patients and their families.
This research has increased our understanding of the basic mechanisms of Alzheimer's disease, allowing us to further understand Alzheimer's disease.
Link to the paper: https:// Open for reprint
Uncovering the mystery of DNA structure for the first time, mankind officially opened the era of molecular biology.
Since then, the iconic double helix structure has become the public's default impression of DNA.
However, as the most important genetic material, is DNA only this kind of structure? In January 2013, Nature Chemistry published a paper, which showed that there is an unusual four-stranded DNA structure in human cells-G-quadruplexes.
On March 23, 2021, researchers from the University of Montreal in Canada published a research paper titled: G-quadruplexes originating from evolutionary conserved L1 elements interfere with neuronal gene expression in Alzheimer's disease in the journal Nature Communications.
The study found that inactivation of the BMI1 gene in human cells or mice can cause heterochromatin relaxation and induce the appearance of G-quadruplex structures.
In neurodegenerative diseases, heterochromatin relaxation in neurons often occurs, and G-quadruplex structures are accumulated in neurons in the brain of Alzheimer's patients.
The study discovered a new function of the BMI1 gene: to prevent the formation of a disordered G-quadruplex structure in the DNA of brain neurons, thereby preventing Alzheimer's disease and inhibiting brain aging.
This research has increased our understanding of the basic mechanisms of Alzheimer's disease, allowing us to further understand Alzheimer's disease.
Alzheimer's disease (AD), commonly known as "Alzheimer's disease", is a serious neurodegenerative disease.
Patients usually suffer from memory decline and weakened learning ability, accompanied by emotional regulation.
Obstacles and loss of athletic ability greatly affect the development of individuals, families and even society.
Currently, about 50 million people worldwide suffer from Alzheimer's disease.
As the average life expectancy of human beings increases and the aging society intensifies, the prevalence of Alzheimer's disease is also rising.
It is estimated that by 2050, Alzheimer's patients will increase to more than 150 million.
Prior to this, the research team published in the journals Cell Reports and Scientific Reports showed that the BMI1 gene has become particularly low in the brains of Alzheimer’s disease patients.
They also found that the BMI1 gene in human neurons and mouse neurons The inactivation is sufficient to generate all the pathological markers associated with Alzheimer's disease.
These findings indicate that the activity of the BMI1 gene is closely related to the onset of Alzheimer's disease, and it is likely to play a function of inhibiting Alzheimer's disease.
In this Nature Communications paper, the research team found that G-quadruplex structures accumulate in the brain neurons of Alzheimer's patients, but not in the brains of healthy elderly people.
Healthy neurons (left), Alzheimer's neurons (right): Green is the accumulation of G4 structures in Alzheimer's neurons.
This study found that inactivation of the BMI1 gene in human cells or mice can lead to heterochromatin Relax and induce the appearance of G-quadruplex structure.
In neurodegenerative diseases, heterochromatin relaxation in neurons often occurs, and G-quadruplex structures are accumulated in neurons in the brain of Alzheimer's patients.
The study discovered a new function of the BMI1 gene: to prevent the formation of a disordered G-quadruplex structure in the DNA of brain neurons, thereby preventing Alzheimer's disease and inhibiting brain aging.
So far, Alzheimer's disease is still incurable.
Therefore, any progress in this field can bring hope to patients and their families.
This research has increased our understanding of the basic mechanisms of Alzheimer's disease, allowing us to further understand Alzheimer's disease.
Link to the paper: https:// Open for reprint
