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Long COVID linked to brain changes and mitochondrial dysfunction, plus new insights on who's most at risk
This week's research reveals some fascinating biological mechanisms behind long COVID symptoms, from how the virus rewires our cells' powerhouses to why certain groups face disproportionate risks. Plus, we're getting clearer pictures of what recovery actually looks like.
🧬 SARS-CoV-2 Spike Protein May Trigger Depression Through Brain Cell Communication
Researchers found that the SARS-CoV-2 spike protein disrupts communication between brain support cells called astrocytes by interfering with gap junctions (tiny channels that let cells talk to each other)
This disruption specifically affects a protein called Cx43, which is crucial for normal brain function and mood regulation
The study provides a potential biological explanation for why depression is such a common and debilitating part of long COVID
Why this matters: This research offers the first clear mechanistic pathway linking the virus directly to depressive symptoms in long COVID patients. Understanding how the spike protein interferes with brain cell communication could lead to targeted treatments that restore normal brain function rather than just managing symptoms.
Also in this issue:
- ⚡ Cellular Powerhouses Show Long COVID Connection
- 🎯 Long COVID Hits Disadvantaged Communities Hardest
- 🧠 Brain Fog Gets More Precise Definition
- 📊 Most Long COVID Patients Don't Recover After a Year
- 🔬 Virus Rewrites Cellular Instruction Manual
- 💊 Daily Stress Worsens Long COVID Symptoms
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