Prodromal network hyperexcitability and mitochondrial dysfunction underly the pathogenesis of various forms of dementia. However, the role of hippocampal hyperexcitability and mitochondria in prodromal dementia with Lewy bodies (DLB) is unclear.We conducted multi-electrode array (MEA) recordings to investigate early hippocampal activity in a transgenic mouse model of DLB which harbours an alanine to proline point mutation (A30P) in the alpha synuclein gene (SNCA), causing overexpression. Hippocampal slices from young pre-symptomatic (2-4 months) male A30P (N = 6 slices/4 mice) and wild-type (WT) (N = 6 slices/3 mice) mice were mounted onto a 400 electrode MEA chip (3Brain), followed by a bath application of kainate or 4-aminopyridine (4-AP) to evoke spiking activity. 4-AP caused a significantly greater increase in the mean spike frequency in slices from A30P mice, compared to WT controls (1.7 and 0.9 spikes/sec respectively, p <0.05) suggesting male A30P mice exhibited hippocampal hyperexcitability.To determine if network hyperexcitability was associated with changes in mitochondria, we used formalin-fixed paraffin embedded hippocampal tissue from young A30P and WT mice. Immunohistochemical staining for mitochondrial Complex I NADH dehydrogenase1 beta subcomplex subunit 8 (NDUFB8), Complex IV mitochondrial encoded cytochrome c oxidase I (MTCO1) and mitochondrial mass (Porin) within parvalbumin interneurons was conducted. Intensity values from NDUFB8 and MTCO1 were normalised to Porin, revealing a trend towards increased expression per mitochondrion.We have demonstrated hippocampal hyperexcitability in young A30P mice, accompanied by a trend towards increased NDUFB8 and MTCO1 expression, possibly reflecting an early compensatory increase in mitochondrial complex I and IV.