Neuroscience MCAT Practice Question
A 34-year-old man with a history of rheumatoid arthritis presents with acute onset headache, fever (38.9°C), and photophobia. MRI brain shows meningeal enhancement. CSF analysis reveals elevated protein (120 mg/dL), normal glucose, and pleocytosis with predominant lymphocytes. Blood cultures are negative, and viral serologies are pending. The patient's serum TNF-α levels are markedly elevated. Over the next 48 hours, his mental status deteriorates despite appropriate antimicrobial coverage. A research team investigating his case notes that TNF-α-mediated blood-brain barrier disruption is likely contributing to increased CNS inflammation. Which of the following best explains the mechanism by which TNF-α compromises blood-brain barrier integrity?
Answer choices
- ATNF-α directly phosphorylates claudins and occludin, causing their immediate internalization and complete loss of tight junction architecture
- BTNF-α binds endothelial cell receptors, activating NF-κB signaling that downregulates tight junction protein expression and increases vascular permeability through increased transcytosis
- CTNF-α increases reactive oxygen species production, which oxidatively damages tight junction proteins and activates matrix metalloproteinases that degrade adhesion moleculesCorrect answer
- DTNF-α directly inhibits Na+/K+-ATPase activity on endothelial cells, causing cellular swelling that physically compresses tight junction proteins
- ETNF-α stimulates pericyte apoptosis, reducing production of angiopoietin-1 and eliminating structural support for endothelial tight junctions
- FTNF-α competitively blocks GLUT1 glucose transporters, reducing ATP production and energy-dependent tight junction protein maintenance
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