Table 2.

Mitochondrial dynamics and neurodegenerative diseases.

Pathology	Proteins involved (expression level and/or mutation)	Mitochondrial phenotype	Mechanisms of pathophysiology involving mitochondria
Alzheimer disease	MFN1, MFN2, OPA1 ↓↓ DRP1, FIS1 ↑↑ KINESIN mutation	Fragmentation, disruption of cristae structure, reduction in number of mitochondria in dendrites, impaired mitochondrial trafficking, defects in KGDH complex, PDH complex and COX.	β amiloyd accumulation and interaction with DRP1, enhanced CDK1 activity, altered interaction between mitochondria and Kinesin motor complex in cerebral cortex [77–79].
Huntington's disease	MFN1, MFN2, OPA1 ↓↓ DRP1, FIS1 ↑↑ HTT mutation	Fragmentation; impaired mitochondrial trafficking, defects in SDH (complex II) and Aconitase.	HTT interaction with DRP1, increased calcineurin and DRP1 activity, redistribution of kinesin and dynein motor complexes in striatal neurons [80–82].
Parkinson disease	Parkin mutation or ↓↓ Pink1 mutation or ↓↓ DJ-1 mutation DRP1 ↓↓ MFN2 α-synuclein mutation LRRK2 mutation	Fragmentation, impaired mitochondrial trafficking.	Altered interaction between mitochondria and motor complexes, impaired mitophagy of damaged mitochondria in substantia nigra [74, 75, 83–86].
Amiotrophic lateral sclerosis	SOD mutation GEFmutation TDP-43 mutation	Fragmentation, disruption of cristae structure with expansion of IMS, impaired mitochondrial trafficking, complex I dysfunctions.	Toxicity associated to the formation of aggregates of mutant SOD, in subsarcolemmal region of muscles and anterior horn neurons of lumbar spinal cord [87–93].
Autosomal dominant optic atrophy	OPA1 mutation	Fragmentation, complex I dysfunctions.	Major sensitivity to death stimuli in retinal ganglion cells and optic nerve [94–98].
Charcot Marie Tooth Type 2	MFN1 mutation GDAP1mutation	Fragmentation (MFN1 mut) or elongation (GDAP1 mut).	MFN1: probably alteration in ER-mitocondria tethering and Calcium signalling [99]; GDAP1: altered localization of GDAP1 [100].