Growth hormone-inducible transmembrane protein (GHITM) is an inner mitochondrial membrane protein that contains the Bax inhibitor-1 motif and is implicated in the regulation of mitochondrial morphology and especially cristae structure. The downregulation of GHITM results in fragmented mitochondria and the release of cytochrome c, while its upregulation delays the release of cytochrome c. We inhibited CG2076 the Drosophila GHITM homologue in the neurons using RNA interference and analysed the phenotypic consequences of this mitochondrial protein. The directed expression of GHITM-RNAi in neurons under the control of the Dopa decarboxylase (Ddc) transgene results in shortened lifespan and impaired climbing ability. The co-expression of Buffy, the only anti-apoptotic B cell lymphoma 2 (Bcl-2) protein in Drosophila, along with GHITM-RNAi results in suppression of the shortened lifespan and premature age-dependent loss in climbing ability. The inhibition of GHITM in the Drosophila eye results in decreased ommatidia number and elevated disruption of the ommatidial array, phenotypes that are rescued upon overexpression of Buffy. The inhibition of the mitochondrial located GHITM in the Ddc-Gal4-expressing neurons of Drosophila results in shortened lifespan and loss in climbing ability, phenotypes that are manifest of degeneration and death of dopaminergic neurons, and are improved upon overexpression of the pro-survival Buffy.