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A healthy mitochondrial network is essential for the maintenance of neuronal synaptic integrity. Mitochondrial and metabolic dysfunction contributes to the pathogenesis of many neurodegenerative diseases including dementia.  OPA1  is the master regulator of mitochondrial fusion and fission and is likely to play an important role during neurodegenerative events. To explore this, we quantified hippocampal dendritic and synaptic integrity and the learning and memory performance of aged  Opa1  haploinsufficient mice carrying the  Opa1 Q285X   mutation (B6; C3- Opa1 Q285STOP  ;  Opa1 +/−  ). We demonstrate that heterozygous loss of  Opa1  results in premature age-related loss of spines in hippocampal pyramidal CA1 neurons and a reduction in synaptic density in the hippocampus. This loss is associated with subtle memory deficits in both spatial novelty and object recognition. We hypothesize that metabolic failure to maintain normal neuronal activity at the level of a single spine leads to premature age-related memory deficits. These results highlight the importance of mitochondrial homeostasis for maintenance of neuronal function during ageing.

OPA1 deficiency accelerates hippocampal synaptic remodelling and age-related deficits in learning and memory