Linking Mitochondria to Neurological Disease



Neurobiology of Disease Webinar and Live Chat

Our understanding of the cell biology of mitochondria has exploded in the last decade, providing a renewed understanding of their contribution to neurological diseases ranging from pediatric encephalomyopathies to Alzheimer’s, Huntington’s, and others.

Select faculty from the 2016 Neurobiology of Disease Workshop will continue the discussion, emphasizing mitochondrial motility and neurodegeneration, mitochondrial function in Alzheimer ’s disease, and the role of mitochondria in immunity and links to neuroinflammation. After the scientific presentations, join all the speakers here in the Neuronline Community for a live chat. Post your questions for the speakers in the replies below. *

In the live chat:

  • Heidi McBride, PhD, professor and Canada Research Chair in Mitochondrial Cell Biology at McGill University
  • Eric Schon, PhD, Lewis P. Rowland Professor of Neurology in genetics and development at Columbia University Medical Center
  • Xinnan Wang, PhD, assistant professor of neurosurgery at Stanford University School of Medicine
  • Phillip West, PhD, assistant professor of microbial pathogenesis and immunology at Texas A&M University Health Science Center

Watch the Webinar: Tuesday, July 18th at 1:00pm (EDT) Register now

Join the Live Chat: Tuesday, July 18th at 1:45pm (EDT) right here in the Neuronline Community

Can’t attend live? Register to watch on-demand.

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We provide evidence that Alzheimer disease is functionally a disorder of ER-mitochondrial communication at contact sites between the two organelles (called mitochondria-associated ER membranes, or MAM), and that the biochemical cause of this altered ER-mitochondrial connectivity is perturbed lipid homeostasis.


Cells balance their energy homeostasis and minimize oxidative stress by regulating mitochondrial function and transport and by eliminating dysfunctional mitochondria. I will give a brief overview of mitochondrial motility and quality control and their implication in neurodegeneration and regeneration.


My presentation will focus on emerging roles for mitochondria in innate immunity and inflammation. I will briefly overview recent advances in the field and relate these findings to the pathobiology of mitochondrial and neurological diseases.


Very interesting. Could you please tell me if, in your opinion, this MAM-miscommunication imply altered calcium signaling? If yes, what kind of alteration? Thank you. Juan F Gomez-Molina, IGN


Has elevated mtDNA ever been observed in the CSF of neurodegenerative disease subjects?


Yes, calcium trafficking is altered. In AD, where ER-mito communication is increased, Ca trafficking from ER to mitos goe up (tyhis has been seen in AD patients and cells).


Do any of you have any thoughts on cause/effect role of lipofuscin granules in the inflammatory and degenerative aspects of brain aging in particular?


Hi! Yes, you can find many papers reporting this in various diseases, and upon infections like HIV. Again, the mechanism of release is not yet established. It’s a new area of investigation for sure.


What is the most likely velocity a mitochondria of a neuron can have, in general? in other words, if we point at random to a mitochondria, should we expect it is moving or resting? thanks…


Yes, I guess the idea is that such granules landing on the cell surface would active innate immune pathway. Not sure it’s been looked at specifically in neurodegeneration.


Great, thanks!


Usually they accumulate inside to a pretty high degree especially in the Hippocampus and Substantia nigra. Are you say you would not expect them to have an immunological effect unless they found their way to the membrane?


anywhere between 0.1-0.5 um/s in experimental systems. at any given time, around 30% of total mitochondria are moving.


Yes, I would so. The TLRs respond to crystals that land on the cell surface, etc., so this could look that that to the receptors.


I appreciate your answer, thanks!


you are welcome!


maybe one more question…is the membrane potential of the inner membrane changing when mitoc moves?


Question from registration:
Mitophagy seems to have exploded from Pink1/Parkin to BNIP Optineurin NDP52 FUNDC3 etc. Are these redundancies or are there specific triggers to these pathways for e.g. pathological vs physiological mitophagy?


some studies suggests that membrane potential may affect the direction of mitochondria move, but other studies suggest otherwise. However, depolarization of membrane potential stops mito because Miro will be degraded.