Mitochondrial and Organellar Crosstalk in Parkinson’s Disease

Bipul Ray, Abid Bhat, Arehally Marappa Mahalakshmi, Sunanda Tuladhar, Muhammed Bishir, Surapaneni Krishna Mohan, Vishnu Priya Veeraraghavan, Ramesh Chandra, Musthafa Mohamed Essa, Saravana Babu Chidambaram*, Meena Kishore Sakharkar

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

10 Citations (Scopus)


Mitochondrial dysfunction is a well-established pathological event in Parkinson’s disease (PD). Proteins misfolding and its impaired cellular clearance due to altered autophagy/mitophagy/pexophagy contribute to PD progression. It has been shown that mitochondria have contact sites with endoplasmic reticulum (ER), peroxisomes and lysosomes that are involved in regulating various physiological processes. In pathological conditions, the crosstalk at the contact sites initiates alterations in intracellular vesicular transport, calcium homeostasis and causes activation of proteases, protein misfolding and impairment of autophagy. Apart from the well-reported molecular changes like mitochondrial dysfunction, impaired autophagy/mitophagy and oxidative stress in PD, here we have summarized the recent scientific reports to provide the mechanistic insights on the altered communications between ER, peroxisomes, and lysosomes at mitochondrial contact sites. Furthermore, the manuscript elaborates on the contributions of mitochondrial contact sites and organelles dysfunction to the pathogenesis of PD and suggests potential therapeutic targets.

Original languageEnglish
JournalASN Neuro
Publication statusPublished - 2021


  • Parkinson’s disease
  • endoplasmic reticulum
  • lysosome
  • mitochondria
  • mitochondrial contact sites
  • peroxisome

ASJC Scopus subject areas

  • General Neuroscience
  • Clinical Neurology


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