HIV and methamphetamine impair human brain-support cells in the lab
HIV or methamphetamine exposure reduced uptake of damaged neurons by 50% compared with untreated human brain-support cells grown in the lab.
Our read
Mechanisms- Studied:
- Experiments in human stem-cell-derived astrocytes, against untreated human brain-support cells
- What changed:
- HIV or methamphetamine exposure reduced uptake of damaged neurons by 50% compared with untreated human brain-support cells
- The catch:
- The mouse experiment measured protein markers rather than brain function
- In the record:
- One of 14 papers on methamphetamine on record: 10 with results in people, 1 in animals.
- Why it’s aging research:
- It studies something that builds up in the body with age.
Editor of record: Boris Djordjevic · AgingResearch.News
Laboratory experiments in human stem-cell-derived astrocytes, cells that support neurons, found that HIV or methamphetamine induced signs of senescence, a state in which cells stop dividing. The cells also made less MEGF10, a receptor that helps them engulf dying neurons, and released more inflammatory signals. Fluid from exposed astrocytes reduced proteins linked to neuronal structure in lab-grown neurons. It also disrupted proteins that join blood-vessel lining cells, allowing more immune cells to cross a laboratory barrier.
Activating β-catenin, a signaling protein, protected astrocytes from senescence and preserved engulfment. Increasing MEGF10 also restored engulfment. In mice carrying transplanted human astrocytes, with four mice per group, HIV, methamphetamine or both increased a senescence marker and reduced MEGF10 in the transplanted cells.
Why it matters
The work addresses how senescence in brain-support cells might contribute to inflammation and neurodegeneration, processes relevant to aging.
Caveats
The functional findings came from cells grown in the lab; the mouse experiment measured protein markers rather than brain function. Neither system tested outcomes in people.
The paper
Rush University Medical Center
Journal of Neuroinflammation, Jun 15, 2026, Open access
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