All articles tagged with #astrocytes
Researchers increased Sox9 to heighten astrocyte activity in mouse models of Alzheimer's, promoting the clearance of amyloid plaques and preserving cognitive function, suggesting a therapy that harnesses the brain’s own support cells to slow dementia progression.
Researchers created a whole-brain 3D map showing that star-shaped astrocytes form extensive, long-distance networks via gap junctions, enabling inter-regional exchange of molecules and displaying plasticity—revealing a hidden, neuron-independent communication substrate that reshapes our understanding of brain organization.
New preclinical work shows astrocytes, when their autophagy pathway is boosted (LC3B/SQSTM1), can clear beta-amyloid in the hippocampus, reducing inflammation and protecting neurons—hinting at a glia-first Alzheimer's therapy. While promising, translating this to humans will require precise delivery, safety assessments, and biomarkers, with trials likely pairing glial agents with other anti-amyloid or anti-inflammatory treatments.
Researchers engineered astrocytes to express a CAR targeting amyloid beta, turning them into brain “super cleaners.” In mice, a single gene-therapy injection either prevented plaque formation when given early or reduced existing amyloid plaques by ~50%, signaling a potential new immunotherapy approach for Alzheimer's—though safety and human trials remain to be established.
A rat study from the University of Technology Sydney links inflammation in the striatum, driven by astrocytes, to more deliberate, goal-directed compulsive actions—challenging the view that compulsions are automatic habits and pointing to anti-inflammatory treatments as potential therapies.
Researchers have identified over 150 DNA control signals in brain cells called astrocytes that may influence Alzheimer's disease, using CRISPRi to study enhancer regions in non-coding DNA, which could lead to new insights and potential treatments for the disease.
Research shows that delivering the protein pleiotrophin (Ptn) to astrocytes in the brain can reverse neural connection and activity changes in mouse models of Down syndrome, suggesting potential for future therapies targeting brain wiring in neurodevelopmental disorders.
Scientists at Cedars-Sinai discovered a new role for astrocytes, called lesion-remote astrocytes (LRAs), which communicate with immune cells to clear debris and promote repair in spinal cord injuries, potentially leading to new treatments for neurological diseases.
The study identifies astrocyte-secreted CCN1 as a key factor in maintaining neural circuit stability in the adult brain, particularly in the visual cortex, by regulating synaptic maturation, inhibitory neuron development, and oligodendrocyte maturation, thereby restricting plasticity and preserving functional connectivity.
The study reveals that lesion-remote astrocytes (LRAs) in the injured spinal cord adopt distinct molecular states that regulate microglia-mediated white matter repair, primarily through CCN1 secretion, which influences microglial lipid metabolism, debris clearance, and neurological recovery. Loss of astrocyte-derived CCN1 impairs debris clearance and functional recovery, positioning LRAs as key orchestrators in CNS repair processes.
Recent research reveals that astrocytes, once considered support cells, play crucial roles in shaping behavior, memory, and health by regulating the environment around neurons, influencing brain functions such as circadian rhythms and memory encoding, and potentially contributing to neurological diseases.
A study in mice shows that increasing the protein Sox9 reactivates brain cells' cleanup functions, reducing Alzheimer's-like plaques and improving memory, suggesting a potential new treatment approach targeting brain maintenance cells called astrocytes.
A study in mice shows that increasing the protein Sox9 reactivates brain cells' cleaning functions, reducing Alzheimer's-like plaques and improving memory, suggesting a potential new treatment approach targeting brain maintenance cells called astrocytes.
Scientists at Weill Cornell Medicine discovered that free radicals produced in astrocytes' mitochondria contribute to dementia, and blocking these radicals with targeted compounds reduced inflammation and protected neurons in animal models, opening new avenues for treatment.
The article discusses how mitochondrial complex III-derived reactive oxygen species (ROS) in astrocytes amplify immune and metabolic changes that contribute to dementia pathology, highlighting the role of specific signaling pathways and potential therapeutic targets.