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Written byNagashiEditor
Wang Duoyu
TypesettingShui Chengwen
Alzheimer's disease (AD) , commonly known as "Alzheimer's disease", is a serious neurodegenerative disease, patients usually appear memory loss, weakened learning ability symptoms, accompanied by emotional regulation disorders and loss of exercise ability, greatly affecting the development of
individuals, families and even society.
Currently, about 50 million people worldwide suffer from Alzheimer's disease
.
As human life expectancy increases and aging society intensifies, the prevalence of Alzheimer's disease is also rising, and it is expected that by 2050, the number of Alzheimer's disease patients will increase to more than
150 million.
In China alone, the incidence of Alzheimer's disease in people over 65 years of age is 5%, and increases by 5%
for each additional 10 years of age.
That is to say, in the 85-year-old population, one in every 2-3 elderly people is Alzheimer's disease, which causes a huge burden
to the family and society.
Therefore, drug development and patient treatment of Alzheimer's disease are essential if the specific cause of Alzheimer's disease is to be revealed
.
On December 13, 2022, researchers at Northwestern University Feinberg School of Medicine published a report on Cell titled: Cerebrospinal Research paper on fluid immune dysregulation during healthy brain aging and cognitive impairment.
The study found that as the elderly age, the cerebrospinal fluid immune system gradually becomes dysfunctional
.
And, in people with cognitive disorders such as Alzheimer's disease, the molecular characteristics of the CSF immune system are very different
from those of healthy individuals.
These results reveal that CSF immune dysregulation may be the culprit responsible for cognitive disorders such as Alzheimer's disease
.
Neuroinflammation is a pathological marker of age-related neurodegenerative diseases, and the cerebrospinal fluid (CSF) immune system is a key factor
in brain immunity.
Recent studies have shown that cerebrospinal fluid provides molecular cues to immune cells in the skull bone marrow to alter the myeloid cell population
in mouse cerebrospinal fluid.
However, scientists still lack understanding
of the molecular mechanisms by which aging regulates the CSF immune system, and how CSF immunity changes with age or neurodegenerative diseases.
Therefore, in this latest study, the research team analyzed the cerebrospinal fluid immune system
of healthy individuals and patients with cognitive impairment through single-cell RNA sequencing technology.
The first part of the study analyzed the cerebrospinal fluid of 45 healthy individuals aged 54-83 years, and the second part compared statistics from the healthy group with the cerebrospinal fluid of 14 people with Alzheimer's disease and cognitive impairment
.
The study design and linear modeling
of changes in CSF immune cell gene expression The research team observed genetic changes in CSF immune cells in healthy older adults that make immune cells become more active with age and lead to inflammation
。 To use a figurative analogy, the cerebrospinal fluid immune cells of the elderly are like an "old urchin" who has lost his temper, and this anger may weaken the function of these cells, resulting in a disorder
of the brain's immune system.
Not only does gene expression
change in cerebrospinal fluid immune cells in healthy older adults with age, but the team also found that in patients with cognitive impairment, the downregulation of monocyte lipid transporter genes was associated with CD8 Cytokine signaling changes in T cells occur
simultaneously.
Clonal CD8 effector memory cells upregulate C-X-C mottagokine receptor 6 (CXCR6)
in patients with cognitive impairment.
Notably, the ligand of CXCR6, C-X-C chemokine ligand 16 (CXCR6), was elevated in the cerebrospinal fluid of cognitively impaired subjects, suggesting that the CXCL16-CXCR6 signaling pathway is the mechanism
by which antigen-specific T cells enter the brain.
These cells have an excess of the cellular receptor, CXCR6, which acts as an antenna, which receives CXCL16 signals from degenerated brain microglia and enters the brain
.
In the cerebrospinal fluid of patients with cognitive impairment, monocytes communicate with CD8+ T cells through the CXCL16-CXCR6 signaling pathway, and these results show that the degenerative brain of patients with cognitive impairment activates antigen-specific T cells.
Let them clone themselves and enter the brain, where these cells are likely to cause damage
because they don't belong there in the first place.
If that's the case, then a strategy could be found to treat cognitive impairment — blocking CXCL16 signaling or inhibiting CXCR6 receptors
.
In the cerebrospinal fluid of people with cognitive dysfunction, clonal dilated T cells cause damage
to the brainAll in all, this study shows that the CSF immune system plays an important role in cognitive disorders such as Alzheimer's disease, It was found that the CXCL16-CXCR6 signaling pathway is the molecular mechanism
by which antigen-specific T cells enter the brain.
These results shed light on cerebrospinal fluid immune dysregulation during healthy brain aging and cognitive impairment, providing a critical foundation
for the diagnosis and treatment of brain inflammation associated with cognitive impairment.
Link to the paper: https://doi.
org/10.
1016/j.
cell.
2022.
11.
019
Open reprint, welcome to forward to Moments and WeChat groups
Wang Duoyu
TypesettingShui Chengwen
Alzheimer's disease (AD) , commonly known as "Alzheimer's disease", is a serious neurodegenerative disease, patients usually appear memory loss, weakened learning ability symptoms, accompanied by emotional regulation disorders and loss of exercise ability, greatly affecting the development of
individuals, families and even society.
Currently, about 50 million people worldwide suffer from Alzheimer's disease
.
As human life expectancy increases and aging society intensifies, the prevalence of Alzheimer's disease is also rising, and it is expected that by 2050, the number of Alzheimer's disease patients will increase to more than
150 million.
In China alone, the incidence of Alzheimer's disease in people over 65 years of age is 5%, and increases by 5%
for each additional 10 years of age.
That is to say, in the 85-year-old population, one in every 2-3 elderly people is Alzheimer's disease, which causes a huge burden
to the family and society.
Therefore, drug development and patient treatment of Alzheimer's disease are essential if the specific cause of Alzheimer's disease is to be revealed
.
On December 13, 2022, researchers at Northwestern University Feinberg School of Medicine published a report on Cell titled: Cerebrospinal Research paper on fluid immune dysregulation during healthy brain aging and cognitive impairment.
The study found that as the elderly age, the cerebrospinal fluid immune system gradually becomes dysfunctional
.
And, in people with cognitive disorders such as Alzheimer's disease, the molecular characteristics of the CSF immune system are very different
from those of healthy individuals.
These results reveal that CSF immune dysregulation may be the culprit responsible for cognitive disorders such as Alzheimer's disease
.
Neuroinflammation is a pathological marker of age-related neurodegenerative diseases, and the cerebrospinal fluid (CSF) immune system is a key factor
in brain immunity.
Recent studies have shown that cerebrospinal fluid provides molecular cues to immune cells in the skull bone marrow to alter the myeloid cell population
in mouse cerebrospinal fluid.
However, scientists still lack understanding
of the molecular mechanisms by which aging regulates the CSF immune system, and how CSF immunity changes with age or neurodegenerative diseases.
Therefore, in this latest study, the research team analyzed the cerebrospinal fluid immune system
of healthy individuals and patients with cognitive impairment through single-cell RNA sequencing technology.
The first part of the study analyzed the cerebrospinal fluid of 45 healthy individuals aged 54-83 years, and the second part compared statistics from the healthy group with the cerebrospinal fluid of 14 people with Alzheimer's disease and cognitive impairment
.
The study design and linear modeling
of changes in CSF immune cell gene expression The research team observed genetic changes in CSF immune cells in healthy older adults that make immune cells become more active with age and lead to inflammation
。 To use a figurative analogy, the cerebrospinal fluid immune cells of the elderly are like an "old urchin" who has lost his temper, and this anger may weaken the function of these cells, resulting in a disorder
of the brain's immune system.
Not only does gene expression
change in cerebrospinal fluid immune cells in healthy older adults with age, but the team also found that in patients with cognitive impairment, the downregulation of monocyte lipid transporter genes was associated with CD8 Cytokine signaling changes in T cells occur
simultaneously.
Clonal CD8 effector memory cells upregulate C-X-C mottagokine receptor 6 (CXCR6)
in patients with cognitive impairment.
Notably, the ligand of CXCR6, C-X-C chemokine ligand 16 (CXCR6), was elevated in the cerebrospinal fluid of cognitively impaired subjects, suggesting that the CXCL16-CXCR6 signaling pathway is the mechanism
by which antigen-specific T cells enter the brain.
These cells have an excess of the cellular receptor, CXCR6, which acts as an antenna, which receives CXCL16 signals from degenerated brain microglia and enters the brain
.
In the cerebrospinal fluid of patients with cognitive impairment, monocytes communicate with CD8+ T cells through the CXCL16-CXCR6 signaling pathway, and these results show that the degenerative brain of patients with cognitive impairment activates antigen-specific T cells.
Let them clone themselves and enter the brain, where these cells are likely to cause damage
because they don't belong there in the first place.
If that's the case, then a strategy could be found to treat cognitive impairment — blocking CXCL16 signaling or inhibiting CXCR6 receptors
.
In the cerebrospinal fluid of people with cognitive dysfunction, clonal dilated T cells cause damage
to the brainAll in all, this study shows that the CSF immune system plays an important role in cognitive disorders such as Alzheimer's disease, It was found that the CXCL16-CXCR6 signaling pathway is the molecular mechanism
by which antigen-specific T cells enter the brain.
These results shed light on cerebrospinal fluid immune dysregulation during healthy brain aging and cognitive impairment, providing a critical foundation
for the diagnosis and treatment of brain inflammation associated with cognitive impairment.
Link to the paper: https://doi.
org/10.
1016/j.
cell.
2022.
11.
019
Open reprint, welcome to forward to Moments and WeChat groups
