Calcium Dynamics in Nuclei and Cytoplasm of Shockwave-Injured Astrocytes from an Alzheimer’s Mouse Model
<p dir="ltr">Alzheimer’s disease (AD) is closely associated with disrupted calcium homeostasis in neurons and glial cells. Astrocytes, essential for regulating calcium signaling in the brain, may contribute to AD progression if their regulatory functions are impaired. This study expl...
Saved in:
| Main Author: | |
|---|---|
| Other Authors: | , , , , , |
| Published: |
2025
|
| Subjects: | |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Summary: | <p dir="ltr">Alzheimer’s disease (AD) is closely associated with disrupted calcium homeostasis in neurons and glial cells. Astrocytes, essential for regulating calcium signaling in the brain, may contribute to AD progression if their regulatory functions are impaired. This study explored calcium dynamics in astrocytes from a PSAPP mouse model of AD, comparing nuclear and cytoplasmic responses following shockwave-induced injury.</p><p dir="ltr">Astrocytes were exposed to laser-induced shockwaves generated by a 1030 nm Coherent laser system, attenuated to deliver controlled single pulses. Cells were stained with Fluo-4 AM to measure calcium responses and Dead-Red to assess viability. Imaging was conducted over 600 frames at 3-second intervals. ImageJ and MATLAB analyses quantified calcium intensity in nuclei and cytoplasm, and statistical tests determined significant differences between groups.</p><p dir="ltr">Results revealed distinct calcium dynamics between live and dead astrocytes. In live cells, nuclei exhibited significantly higher average peak brightness compared to cytoplasm, indicating compartmental regulation. Dead nuclei, in contrast, showed lower calcium responses than dead cytoplasm. Statistical comparisons confirmed significant differences in live cytoplasm versus nuclei (p = 0.03981), while differences in dead cells were not significant. These findings suggest that AD astrocytes lose compartment-specific calcium regulation under stress, impairing their ability to maintain cellular homeostasis.</p><p dir="ltr">The study concludes that abnormal calcium compartmentalization contributes to astrocytic dysfunction in AD. Expanding this work to include wild-type astrocytes will be essential to validate these findings and clarify their role in AD pathology. Insights gained could inform therapeutic approaches targeting astrocytic calcium regulation.</p> |
|---|