Mitochondria are essential for synaptic activity and plasticity, providing energy, buffering calcium, and recycling vesicles needed for neurotransmission. Presynaptic mitochondria support rapid neurotransmitter release, while postsynaptic mitochondria buffer calcium for sustained activity. Mitochondrial plasticity, their ability to adapt to neuronal demands, is critical but not fully understood. Dysfunctions in mitochondrial dynamics, such as fission and fusion, disrupt energy production and calcium balance, contributing to neurodegenerative diseases like Alzheimer’s (AD). In AD, mitochondrial impairment exacerbates amyloid-beta and tau accumulation, leading to further synaptic damage.

Future research should clarify the relationship between mitochondrial and synaptic plasticity to understand the sequence of dysfunction. Advanced imaging and molecular tools can reveal how mitochondrial dynamics affect synaptic alterations. Potential interventions include gene therapy for mitochondrial defects, targeting fission and fusion imbalances, and improving mitochondrial transport. Early detection of mitochondrial dysfunction could prevent or slow neurodegeneration, offering new therapeutic strategies to preserve neuronal health and combat conditions like AD.

Reference: Sayehmiri F, Motamedi F, Batool Z, et al. Mitochondrial plasticity and synaptic plasticity crosstalk; in health and Alzheimer’s disease. CNS Neurosci Ther. 2024 Aug;30(8):e14897. doi: 10.1111/cns.14897. PMID: 39097920; PMCID: PMC11298206.