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Mitochondrial and Endoplasmic Reticulum Stress Trigger Triglyceride Accumulation in Models of Parkinson’s Disease Independent of Mutations in MAPT

Metabolites, ISSN: 2218-1989, Vol: 13, Issue: 1
2023
  • 5
    Citations
  • 0
    Usage
  • 5
    Captures
  • 2
    Mentions
  • 8
    Social Media
Metric Options:   Counts1 Year3 Year

Metrics Details

  • Citations
    5
  • Captures
    5
  • Mentions
    2
    • Blog Mentions
      1
      • Blog
        1
    • News Mentions
      1
      • News
        1
  • Social Media
    8
    • Shares, Likes & Comments
      8
      • Facebook
        8

Most Recent Blog

Metabolites, Vol. 13, Pages 112: Mitochondrial and Endoplasmic Reticulum Stress Trigger Triglyceride Accumulation in Models of Parkinson’s Disease Independent of Mutations in MAPT

Metabolites, Vol. 13, Pages 112: Mitochondrial and Endoplasmic Reticulum Stress Trigger Triglyceride Accumulation in Models of Parkinson’s Disease Independent of Mutations in MAPT Metabolites doi:

Most Recent News

New Parkinson's Disease Findings from University of Cambridge Published (Mitochondrial and Endoplasmic Reticulum Stress Trigger Triglyceride Accumulation in Models of Parkinson's Disease Independent of Mutations in MAPT)

2023 FEB 08 (NewsRx) -- By a News Reporter-Staff News Editor at Genomics & Genetics Daily -- Research findings on Parkinson's disease are discussed in

Article Description

The metabolic basis of Parkinson’s disease pathology is poorly understood. However, the involvement of mitochondrial and endoplasmic reticulum stress in dopamine neurons in disease aetiology is well established. We looked at the effect of rotenone- and tunicamycin-induced mitochondrial and ER stress on the metabolism of wild type and microtubule-associated protein tau mutant dopamine neurons. Dopamine neurons derived from human isolated iPSCs were subjected to mitochondrial and ER stress using RT and TM, respectively. Comprehensive metabolite profiles were generated using a split phase extraction analysed by reversed phase lipidomics whilst the aqueous phase was measured using HILIC metabolomics. Mitochondrial and ER stress were both shown to cause significant dysregulation of metabolism with RT-induced stress producing a larger shift in the metabolic profile of both wild type and MAPT neurons. Detailed analysis showed that accumulation of triglycerides was a significant driver of metabolic dysregulation in response to both stresses in both genotypes. Whilst the consequence is similar, the mechanisms by which triglyceride accumulation occurs in dopamine neurons in response to mitochondrial and ER stress are very different. Thus, improving our understanding of how these mechanisms drive the observed triglyceride accumulation can potentially open up new therapeutic avenues.

Bibliographic Details

Fernandes, Hugo J R; Kent, Josh P; Bruntraeger, Michaela; Bassett, Andrew R; Koulman, Albert; Metzakopian, Emmanouil; Snowden, Stuart G

MDPI AG

Medicine; Biochemistry, Genetics and Molecular Biology

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