Scientists Uncover New Mechanism for Brain Self-Repair After Stroke
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Scientists Uncover New Mechanism for Brain Self-Repair After Stroke
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Scientists Uncover New Mechanism for Brain Self-Repair After Stroke.
Researchers have identified a novel molecular pathway that triggers self-repair in injured brain cells following ischemic stroke.
This discovery holds promise for limiting or reversing damage caused by ischemic stroke and promoting recovery.
Ischemic stroke, the most common type of stroke, occurs when blood clots or fatty deposits block arteries leading to the brain, cutting off blood and oxygen supply to a specific region, resulting in brain cell damage or death.
After an ischemic stroke, individuals often regain partial lost brain functions through enhanced rehabilitation therapies, indicating the brain’s capacity for self-restoration.
However, the underlying mechanisms of neural recovery have remained elusive until now.
It is well-known that various lipids produced after tissue injury can modulate inflammation in the aftermath of damage.
Consequently, researchers at Tokyo Medical and Dental University focused on this aspect.
Lead author of the study, Takashi Shichita, stated, “Evidence suggests that more lipids are produced after tissue injury, contributing to inflammation regulation.
We investigated alterations in lipid metabolites generated within mice following ischemic stroke.
Interestingly, levels of a specific fatty acid called dihomo-γ-linolenic acid (DGLA) and its derivatives increased after the stroke.”
DGLA belongs to the ω-6 fatty acid family and possesses known anti-inflammatory properties.
Upon deeper investigation, researchers discovered that PLA2GE2 (Phospholipase A2 Group IIE) regulates the release of DGLA.
By manipulating the expression of PLA2GE2 within mice, they found it impacted brain cell recovery.
Lack of this enzyme led to heightened inflammation, reduced expression of neuronal repair stimuli factors, and increased tissue loss.
This finding propelled researchers to further explore brain restoration pathways.
“When we examined gene expression in mice lacking PLA2GE2, we found significantly lower levels of a protein called peptidyl arginine deiminase 4 (PADI4),” noted the study’s first author, Akari Nakamura.
“PADI4 regulates the transcription of genes involved in brain repair and inflammation response.
Importantly, expressing PADI4 in mice limited the extent of tissue damage and inflammation after ischemic stroke!”
From DGLA to PLA2GE2 and then to PADI4, researchers mapped out the entire signaling pathway involved in brain repair.
While this study utilized a mouse model, researchers found that in humans, neurons around stroke-affected areas express PLA2GE2 and PADI4, indicating the presence of a similar recovery pathway within our bodies.
The researchers noted that uncovering this novel mechanism triggering brain repair could lead to the development of therapies that enhance the action of PADI4, expediting recovery after ischemic stroke.
DGLA is present in plant oils, grains, most meats, and dairy products. Accumulation in the brain after ingestion suggests that dietary intervention might prevent post-stroke neural damage.
Currently, only ω-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have gained popularity as nutritional supplements due to their anti-inflammatory properties and cardiovascular risk reduction capabilities.
“While detailed clinical research is still required, our findings might challenge the prevailing notion that only EPA or DHA are beneficial in preventing atherosclerosis and vascular diseases.”
This study was published in the journal “Neuron.”
Scientists Uncover New Mechanism for Brain Self-Repair After Stroke
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