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Written byWang CongEditorWang Duoyu TypesettingThe brains of mammals showed
remarkable stability
over a period of several years to decades.
Due to the brain's limited regenerative capacity, neurons must faithfully perform their functions
throughout the animal's life.
However, as we age, the longevity of neurons makes the brain sensitive
to damage that accumulates over time.
This neuronal damage, combined with age-dependent changes in non-neuronal cells that support neural circuit function, is thought to lead to decreased brain function and an increased
risk of neurodegenerative diseases associated with aging.
An important hypothesis for brain aging is that changes in neuronal and synaptic function associated with age and neurodegeneration are the result of disruption of the brain's homeostatic environment.
In the brain, neurons are supported by a large number of non-neuronal cells, each of which maintains different aspects
of tissue homeostasis.
For example, oligodendrocytes sheath axons and provide metabolic support to neurons; Astrocytes provide nutritional and ionic support to neurons and regulate synaptic function; Microglia provide immune monitoring, synaptic pruning, and phagocytosis clearance of debris
.
Brain damage, infection, and neurodegeneration have been shown to trigger inflammatory activation of these non-neuronal cell types and recruit peripheral immune cells to have protective or harmful effects
on neighboring neurons.
Recent transcriptomic studies of normal brain aging and neurodegenerative diseases, as well as studies of specific non-neuronal cell types, such as astrocytes, microglia, and endothelial cells, have further highlighted the role of
inflammatory activation in aging-related decline.
In particular, reaction states normally triggered in microglia and astrocytes during brain infection or injury also appear
during normal aging.
While these studies show that the widespread disruption of age-related brain homeostasis manifests itself in a variety of cell types, it also raises a number of questions
Answering these questions is challenging because the brain's sheer cell count and molecular complexity hinder our comprehensive understanding of
how the brain changes over its lifetime.
Recently, Xiaowei Zhuang's team at Harvard University published a research paper in Cell entitled: Molecular and spatial signatures of mouse brain aging at single-cell resolution
。
This study developed an experimental method combining single-cell transcriptional composition, multiplex fault-tolerant fluorescence in situ hybridization (MERFISH), and single-cell nuclear transcriptome sequencing (snRNA-seq).
A systematic description
of changes in cellular molecular characteristics and spatial organization during brain aging.
Using this method, it is possible to analyze gene expression and identify cell types and states in the frontal cortex and layers of mice, resulting in spatially resolved cell maps
of these regions of different ages.
This high-resolution cell atlas reveals age-related changes in neuronal and non-neuronal cells and reveals molecular and spatial signatures
of glial and immune cell activation during aging.
Comparison with lipopolysaccharide (LPS)-induced changes further reveals unknown differences
in non-neuronal cell activation induced by aging and systemic inflammatory stimuli.
The diversity and complex organization of cells in the brain hinders the systematic description of age-related changes in its cellular and molecular structure, limiting our ability to understand the mechanisms of declining brain function during aging.
The research team used spatially resolved single-cell transcriptomics to generate high-resolution maps of brain senescent cells in the frontal cortex and striatum, and quantified changes
in gene expression and spatial organization of major cell types in these regions during mouse lifetime.
The research team observed significant changes in cell state, gene expression, and spatial organization of non-neuronal cells.
These research data reveal the molecular and spatial signatures of glial and immune cell activation during aging, particularly in subcortical white matter, and identify similarities and significant differences
in cell activation patterns induced by aging and systemic inflammatory stimuli.
These results provide important insights
into age-related decline and inflammation in the brain.
Link to the paper: https://doi.
org/10.
1016/j.
cell.
2022.
12.
010
Open reprint, welcome to forward to Moments and WeChat groups
remarkable stability
over a period of several years to decades.
Due to the brain's limited regenerative capacity, neurons must faithfully perform their functions
throughout the animal's life.
However, as we age, the longevity of neurons makes the brain sensitive
to damage that accumulates over time.
This neuronal damage, combined with age-dependent changes in non-neuronal cells that support neural circuit function, is thought to lead to decreased brain function and an increased
risk of neurodegenerative diseases associated with aging.
An important hypothesis for brain aging is that changes in neuronal and synaptic function associated with age and neurodegeneration are the result of disruption of the brain's homeostatic environment.
In the brain, neurons are supported by a large number of non-neuronal cells, each of which maintains different aspects
of tissue homeostasis.
For example, oligodendrocytes sheath axons and provide metabolic support to neurons; Astrocytes provide nutritional and ionic support to neurons and regulate synaptic function; Microglia provide immune monitoring, synaptic pruning, and phagocytosis clearance of debris
.
Brain damage, infection, and neurodegeneration have been shown to trigger inflammatory activation of these non-neuronal cell types and recruit peripheral immune cells to have protective or harmful effects
on neighboring neurons.
Recent transcriptomic studies of normal brain aging and neurodegenerative diseases, as well as studies of specific non-neuronal cell types, such as astrocytes, microglia, and endothelial cells, have further highlighted the role of
inflammatory activation in aging-related decline.
In particular, reaction states normally triggered in microglia and astrocytes during brain infection or injury also appear
during normal aging.
While these studies show that the widespread disruption of age-related brain homeostasis manifests itself in a variety of cell types, it also raises a number of questions
- How do molecular signatures and spatial organization of different cell types and cell states change with age, and how do these changes relate to age-induced inflammatory activation?
- How are activated cells spatially distributed?
- Does this activation depend on environmental factors and cell-to-cell communication?
- How does age-related inflammation relate to systemic inflammatory response?
Answering these questions is challenging because the brain's sheer cell count and molecular complexity hinder our comprehensive understanding of
how the brain changes over its lifetime.
Recently, Xiaowei Zhuang's team at Harvard University published a research paper in Cell entitled: Molecular and spatial signatures of mouse brain aging at single-cell resolution
。
This study developed an experimental method combining single-cell transcriptional composition, multiplex fault-tolerant fluorescence in situ hybridization (MERFISH), and single-cell nuclear transcriptome sequencing (snRNA-seq).
A systematic description
of changes in cellular molecular characteristics and spatial organization during brain aging.
Using this method, it is possible to analyze gene expression and identify cell types and states in the frontal cortex and layers of mice, resulting in spatially resolved cell maps
of these regions of different ages.
This high-resolution cell atlas reveals age-related changes in neuronal and non-neuronal cells and reveals molecular and spatial signatures
of glial and immune cell activation during aging.
Comparison with lipopolysaccharide (LPS)-induced changes further reveals unknown differences
in non-neuronal cell activation induced by aging and systemic inflammatory stimuli.
The diversity and complex organization of cells in the brain hinders the systematic description of age-related changes in its cellular and molecular structure, limiting our ability to understand the mechanisms of declining brain function during aging.
The research team used spatially resolved single-cell transcriptomics to generate high-resolution maps of brain senescent cells in the frontal cortex and striatum, and quantified changes
in gene expression and spatial organization of major cell types in these regions during mouse lifetime.
The research team observed significant changes in cell state, gene expression, and spatial organization of non-neuronal cells.
These research data reveal the molecular and spatial signatures of glial and immune cell activation during aging, particularly in subcortical white matter, and identify similarities and significant differences
in cell activation patterns induced by aging and systemic inflammatory stimuli.
These results provide important insights
into age-related decline and inflammation in the brain.
Link to the paper: https://doi.
org/10.
1016/j.
cell.
2022.
12.
010
Open reprint, welcome to forward to Moments and WeChat groups
