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A new mechanism for motor-learning circuit rewiring

To address this question, the researchers used mouse models undergoing repeated motor training tasks, including the rotarod test, which measures motor coordination and learning. Using advanced imaging tools that can track individual synaptic components, the team observed a marked increase in astrocyte-mediated synapse elimination as motor learning progressed. In contrast, other glial cell types, such as microglia and oligodendrocyte precursor cells, showed no significant changes under the same experimental conditions, indicating a specific role for astrocytes in this process.

The researchers identified MEGF10, a phagocytic receptor expressed in astrocytes, as a key molecular mediator of this remodeling. When MEGF10 was selectively deleted in astrocytes, mice exhibited impaired motor learning and significant disruptions in communication between the motor cortex and the striatum. In addition, both long-term potentiation (LTP) and long-term depression (LTD)—two fundamental mechanisms of synaptic plasticity—were compromised. These results demonstrate that astrocyte-mediated synapse elimination is not merely a housekeeping function, but a necessary component of functional circuit refinement during learning.

The team further investigated how astrocytes determine which synapses to remove and identified two major regulatory signals. First, increasing neuronal activity between the motor cortex and the striatum significantly enhanced astrocyte-mediated synaptic elimination (a process in which astrocytes engulf and remove synapses), indicating that circuit engagement promotes remodeling. Second, manipulating dopamine levels, a key neuromodulator for movement and reward, also strongly influenced astrocytic synapse elimination. ScienceMission sciencenewshighlights.


When we learn a new motor skill—whether mastering a piano passage or refining balance while walking—the brain must reorganize the circuits that control movement. For decades, this process of synaptic remodeling has been attributed primarily to neurons strengthening or weakening their connections. However, the new study reveals that another cell type in the brain called astrocytes actively participates in this rewiring process.

A research team has demonstrated that astrocytes actively eliminate synapses in the striatum, a brain region that plays a central role in controlling voluntary movement and learning. This process is regulated by dopamine signaling and neural activity and is critical for proper motor skill acquisition.

Although synapse formation and elimination have long been studied in the context of neuronal plasticity, increasing evidence suggests that glial cells—particularly astrocytes and microglia—also contribute to synapse turnover. Until now, however, the precise role of astrocytes in motor learning and the mechanisms underlying their synaptic remodeling remained unclear.

Decoding alzheimer’s: The role of EEG rhythms and aperiodic components in cognitive decline

[Alzheimer’s disease: AD] Zhang et al.: “Increased theta band power was statistically significant in AD patients, highlighting its critical role in AD pathology.”


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A strategy of microglia replacement alleviates microgliopathy in a CSF1R I794T hotspot mutation mouse model of CSF1R-related disorder

Microglial replacement strategy to treat microgliopathy.

Colony-stimulating factor 1 receptor (CSF1R) gene mutation (I794T) is linked to primary microgliopathy manifesting as leukoencephalopathy.

The researchers define the clinical features of patients carrying the CSF1R p. I794T variant and establish a corresponding knockin mouse model.

The authors demonstrate that knockin mice exhibited hallmark features of CSF1R-related disorder (CSF1R-RD).

They show that Csf1rI792T/+ microglia adopt a disease associated state and that a microglial replacement strategy termed “duplicate-cyclic microglial depletion for transplantation” (DCMDT), mitigates cognitive and neuropathological deficits in CSF1R-RD. sciencenewshighlights ScienceMission https://sciencemission.com/microglia-replacement-18450


Li et al. define the clinical features of patients carrying the CSF1R p. I794T variant and establish a corresponding knockin mouse model. They show that Csf1rI792T/+ microglia adopt a disease-associated state and that a microglial replacement strategy, DCMDT, mitigates cognitive and neuropathological deficits in CSF1R-related disorder.

The structure of consciousness

The nature of human experience, or consciousness, has divided thinkers for centuries. The Scottish philosopher Hume saw experience as nothing more than a bundle of perceptions, and denied the existence of a self holding them all together. Kant disagreed, arguing that sensation had to be organised by concepts for there to be experience. It is a debate that has echoed through the Western tradition. You might think science would have settled the matter, but the same dispute is still present amongst neuroscientists. Some argue that sensation is independent of how we think, a neutral bedrock of data which enables us to experience reality. While others claim what we take to be reality is an illusion created by our brain. Do our thoughts and concepts shape and structure experience and what we take to be reality? Are current theories of neuroscience taking sides in this deeper underlying philosophical dispute? Does the existence of the self and the nature of reality depend on our philosophical outlook, or is there a fact of the matter that we might uncover?

Handwriting vs. typing: 30 brain studies reveal which is better for your brain

From the article:

“A review of brain imaging studies found that handwriting activates a broader network of neural pathways than typing or tapping, engaging fine motor skills, memory encoding, and deeper cognitive processing simultaneously. The physical act of forming letters on paper recruits brain regions that digital input simply doesn’t reach. Studies suggest that the pen engages what some researchers describe as a “symphony of neural pathways,” connecting motor control to thought formation in ways that keyboards and touchscreens may bypass.”

Scientists Find Protein Inside The Body That Reverses Brain Aging

Cyclin D-binding myb-like transcription factor 1 or DMTF1a key protein in the brain can help to regenerate neural stem cells and improve aging-associated memory decline. NUS scientists found that this protein’s levels are repressed in the “aged” neural stem cells, Health & Wellness News, Health and Me

Tubulin prevents toxic protein clumps in the brain, fighting back against neurodegeneration

Researchers at Baylor College of Medicine have discovered a potential new strategy to fight back against Alzheimer’s and Parkinson’s diseases, conditions that are linked to the toxic accumulation of Tau and alpha synuclein protein clumps in the brain. The team reports in Nature Communications that tubulin, the building block of microtubules, the cell’s internal ‘railway tracks, can stop Tau and alpha synuclein from forming toxic clumps and instead steer them into their normal, healthy roles.

“Tau and alpha synuclein are well known for their roles in neurodegenerative diseases like Alzheimer’s and Parkinson’s. In these conditions, these proteins can misfold, stick together and form harmful aggregates that damage neurons and contribute to memory loss, movement problems and other symptoms,” said first author Dr. Lathan Lucas, postdoctoral associate of biochemistry and molecular pharmacology in Dr. Allan Ferreon’s lab.

“But Tau and alpha synuclein also fulfill essential functions in healthy neurons—they help maintain cell structure and support communication by interacting with tubulin and contributing to microtubule assembly and stabilization.”

Tubulin Cytoskeleton in Neurodegenerative Diseases–not Only Primary Tubulinopathies

Neurodegenerative diseases represent a large group of disorders characterized by gradual loss of neurons and functions of the central nervous systems. Their course is usually severe, leading to high morbidity and subsequent inability of patients to independent functioning. Vast majority of neurodegenerative diseases is currently untreatable, and only some symptomatic drugs are available which efficacy is usually very limited. To develop novel therapies for this group of diseases, it is crucial to understand their pathogenesis and to recognize factors which can influence the disease course. One of cellular structures which dysfunction appears to be relatively poorly understood in the light of neurodegenerative diseases is tubulin cytoskeleton.

Mitochondrial Ca2+ efflux controls neuronal metabolism and long-term memory across species

Mitochondrial calcium regulates neuronal metabolism and memory.

Brain metabolism is important for long-term memories (LTMs) and various brain functions, Although it is well known that impairing neuronal metabolism limits brain performance, it is not clear if expanding the metabolic capacity of neurons boosts brain function.

In this study, the authors demonstrate that increasing mitochondrial metabolism can enhance LTM formation in flies and mice.

The authors increase mitochondrial Ca2+ by knocking down the mitochondrial Ca2+ exporter Letm1 and demonstrate over-activation of mitochondrial metabolism in neurons of central memory circuits, leading to improved LTM storage. sciencenewshighlights Science Mission https://sciencemission.com/Mitochondrial-Ca2-efflux


Boosting mitochondrial metabolism in neurons in central memory circuits by enhancing Ca2+ retention in the mitochondrial matrix is shown to improve long-term memory formation in flies and mice.

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