Scientists discover never-before-seen type of brain cell

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https://www.livescience.com/health/neuroscience/scientists-discover-never-before-seen-type-of-brain-cell?utm_medium=referral&utm_source=pushly&utm_campaign=Clicked%20Last%2090

1st March, 2025

Scientists have identified a never-before-seen type of cell that may help to heal brain damage — at least in mice.

The researchers discovered a unique kind of astrocyte, a star-shaped cell that supports communication between brain cells, or neurons, and keeps them healthy by stabilizing the brain's protective barrier and regulating neurons' balances of charged particles and signalling molecules.

In the brain, astrocytes either live in gray matter, which contains the main part of neurons that holds DNA and enables the cells to process information, or white matter — the insulated wires that extend from some neurons. Researchers have long-studied the role of gray-matter astrocytes, but until now, less was known about their white-matter counterparts.

In the new study, published Monday (Feb. 24) in the journal Nature Neuroscience, scientists determined the function of white-matter astrocytes in tissue samples from the brains of mice. They did this by analyzing the activity of the genes these cells expressed, or "switched on."

The new study changes our understanding of the role of supportive cells known as astrocytes in the brain. (Image credit: JUAN GAERTNER/SCIENCE PHOTO LIBRARY via Getty Images):

[smfadmin]

The  researchers discovered a unique kind of astrocyte, a star-shaped cell that supports communication between brain cells, or neurons, and keeps them healthy by stabilizing the brain's protective barrier and regulating neurons' balances of charged particles and signalling molecules.

In the brain, astrocytes either live in gray matter, which contains the main part of neurons that holds DNA and enables the cells to process information, or white matter — the insulated wires that extend from some neurons.

Researchers have long-studied the role of gray-matter astrocytes, but until now, less was known about their white-matter counterparts.

In the new study, published Monday (Feb. 24) in the journal Nature Neuroscience, scientists determined the function of white-matter astrocytes in tissue samples from the brains of mice.

They did this by analyzing the activity of the genes these cells expressed, or "switched on."

"That is a really important finding because that wasn't known before," study co-author Judith Fischer-Sternjak, the deputy director of the Institute of Stem Cell Research at Helmholtz Munich in Germany, told Live Science.


The new study, published June 11 in the journal PLOS Pathogens, suggests that one of these hideouts is in brain cells called astrocytes. Astrocytes constitute roughly 60% of the total cells in the human brain, according to the report, and in an infected person, the study authors estimate that between 1% and 3% of these cells could harbor HIV:

https://cdn.jwplayer.com/previews/eoEY9V1y

[Chip (OP)]

Related:

CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model

Abstract

Astrocytes promote neuroinflammation and neurodegeneration in multiple sclerosis (MS) through cell-intrinsic activities and their ability to recruit and activate other cell types. In a genome-wide CRISPR-based forward genetic screen investigating regulators of astrocyte proinflammatory responses, we identified the C-type lectin domain-containing 16A gene (CLEC16A), linked to MS susceptibility, as a suppressor of nuclear factor-κB (NF-κB) signaling. Gene and small-molecule perturbation studies in mouse primary and human embryonic stem cell-derived astrocytes in combination with multiomic analyses established that CLEC16A promotes mitophagy, limiting mitochondrial dysfunction and the accumulation of mitochondrial products that activate NF-κB, the NLRP3 inflammasome and gasdermin D. Astrocyte-specific Clec16a inactivation increased NF-κB, NLRP3 and gasdermin D activation in vivo, worsening experimental autoimmune encephalomyelitis, a mouse model of MS. Moreover, we detected disrupted mitophagic capacity and gasdermin D activation in astrocytes in samples from individuals with MS. These findings identify CLEC16A as a suppressor of astrocyte pathological responses and a candidate therapeutic target in MS.