{
  "id": 2934572,
  "title": "Mitochondrial Metabolism and Calcium Handling in Parkinsons Disease hiPSC-derived Astrocytes",
  "url": "https://urgent.news/2026/08/17/mitochondrial-metabolism-and-calcium-handling-in-parkinsons-disease",
  "topic": "science",
  "section": "Science",
  "published": "2026-08-17T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.08.07.743508v1?rss=1"
  },
  "original_language": "en",
  "account": "Parkinson's disease (PD) is a prevalent neurodegenerative disorder, with mutations in the LRRK2 and PRKN genes being among the most common familial causes. Deviations in calcium homeostasis and cellular bioenergetics in neurons and glial cells, such as astrocytes, impair neuron function and contribute to disease progression. This study focuses on mitochondrial dysfunction and disrupted calcium homeostasis in hiPSC-derived astrocytes with PD gene mutations, comparing them to wild-type controls.\n\nIntracellular calcium dynamics were evaluated using Fura-2 AM. LRRK2-related PD patient-derived mutant astrocytes displayed reduced intracellular calcium levels, and slower calcium extrusion following ATP stimulation. Mitochondrial morphology was analyzed using MitoTracker Deep Red, which revealed increased mitochondrial fragmentation and a shift of mitochondria towards the cell periphery in both PD mutant cell types.\n\nThe study further examined oxygen consumption rates and quantified genes and proteins involved in mitochondrial calcium transport and bioenergetics using a continuous metabolic monitoring system (Resipher) and RT-qPCR, along with capillary electrophoresis-based western detection. The results showed that PRKN mutant astrocytes exhibited a more oxidative bioenergetic phenotype than LRRK2 mutant astrocytes. Both mutant lines displayed altered phosphorylation of the mitochondrial morphology regulator DRP1 and decreased levels of respiratory complexes compared to control astrocytes.\n\nIn conclusion, this research identifies glial-specific mitochondrial dysfunctions and calcium dysregulation as crucial aspects of LRRK2- and PRKN-related pathology. These findings offer new insights into how glial metabolic alterations contribute to neurodegeneration in PD.",
  "summary": "Parkinsons disease (PD) is the second most common neurodegenerative disorder worldwide, and mutations in the LRRK2 and PRKN genes are among the most common familial causes of the disease. In neurodegenerative diseases such as PD, disturbances in Ca{superscript 2} homeostasis and cellular bioenergetics impair the function of neurons and glial cells, contributing to disease progression. These…",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}