All articles tagged with #microglia
Age-related slowdown of neuronal protein recycling leads to protein clumps at synapses; microglia attempt cleanup but can become overwhelmed, potentially impairing neuron communication and linking aging to synaptic loss and higher neurodegenerative risk, with new targets for therapy and biomarkers suggested.
Researchers at Cold Spring Harbor Laboratory found that inhibiting the enzyme PTP1B improves brain microglial function and helps clear amyloid-β plaques in mice, potentially slowing memory decline in Alzheimer's disease. The study suggests PTP1B inhibitors could be paired with existing therapies, with ongoing work to develop such inhibitors for clinical use.
In a mouse model of Alzheimer’s disease, researchers found that inhibiting the brain enzyme PTP1B enhances microglial clearance of amyloid-beta by boosting SYK signaling, improving learning and memory. Because PTP1B is already a target for metabolic disorders, this approach could complement existing amyloid-clearing therapies and pave the way for combination treatments to slow disease progression.
A mouse study shows tumors releasing cystatin-C into the bloodstream can cross the blood-brain barrier, bind amyloid-beta, and activate microglia via Trem2 to clear plaques, sometimes improving memory in Alzheimer’s-like mice. While intriguing, these results are in animals and it's unknown whether humans would experience a similar protective effect; researchers are exploring therapies that mimic this mechanism without cancer.
A mouse study found that human tumors implanted in Alzheimer’s-model mice released cystatin-C into the bloodstream, which crossed the blood–brain barrier and bound to amyloid-beta plaques. This activated brain microglia via Trem2, boosting plaque clearance and sometimes improving memory. While intriguing as a potential pathway to treat or prevent Alzheimer’s, the findings are in mice and may not translate to humans, where cancer and Alzheimer's have a complex, inverse epidemiological relationship. Future work may explore therapies that mimic cystatin-C’s beneficial effects without cancer.
In a mouse study, tumors produced the protein cystatin-C, which traveled to the brain, bound toxic amyloid oligomers, and activated microglia via the TREM2 receptor to clear plaques, improving cognitive tasks. While promising as a novel research path beyond amyloid-lowering strategies, whether these effects translate to humans remains unknown and more work is needed; the study warns against pursuing cancer as a therapy and emphasizes early-stage findings.
New research suggests infantile amnesia isn’t a glitch but a feature: microglia, the brain’s immune cells, prune developing synapses and erase early memories. In infant mice, inhibiting microglial activity with minocycline prevented forgetting of a fear memory, eight days after learning, while memory engrams remained detectable, indicating the memories were stored but typically scrubbed during development.
Researchers discovered that two types of brain immune cells, microglia, act as internal 'accelerators' and 'brakes' to regulate anxiety levels in mice, suggesting new avenues for understanding and treating anxiety disorders in humans.
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.
A new study suggests that specific immune cells in the brain called microglia can switch to a protective state that may prevent or slow Alzheimer's disease progression, opening potential avenues for immunotherapy. The research highlights the importance of microglia's plasticity and their role in combating harmful protein buildup associated with Alzheimer's, with implications for future treatments targeting immune cell states.
Scientists have identified a unique group of microglia with lower PU.1 levels and higher CD28 expression that can protect the brain by reducing inflammation and slowing Alzheimer's pathology, opening new avenues for immunotherapy.
The study investigates how lymphoid gene expression supports neuroprotective functions of microglia in the human brain, particularly in the context of Alzheimer's disease, using post-mortem samples, induced pluripotent stem cells, and mouse models to explore microglial roles and gene regulation.
A study in mice suggests that engineered 'young' immune cells can partly reverse Alzheimer's symptoms and improve brain health by reducing inflammation and supporting memory-related cells, although further research is needed to confirm effects in humans.
Scientists at McGill University have identified two specific types of brain cells—excitatory neurons and microglia—that show changes in individuals with depression, providing new insights into the biological basis of the condition and potential targets for treatment.
Scientists developed a new imaging method revealing that immune cells in the eye become hyperactive early in diabetic retinopathy, before visible damage occurs. The drug liraglutide normalizes this activity, offering potential for early diagnosis and treatment to prevent blindness.