This treatment is currently in active clinical trials. A γ-secretase inhibitor of Notch signaling was shown to induce new hair cells and partially recover hearing loss. Auditory hair cell loss is permanent damage due to the inability of these cells to regenerate. Therefore, deafness due to this pathology is viewed as irreversible. Hair cell development is mediated by Notch signaling, which exerts lateral inhibition onto hair cells. Notch signaling in supporting hair cells leads to prevention of differentiation in surrounding hair cells. After identifying a potent γ-secretase inhibitor selective for stimulating differentiation in inner ear stem cells, it was administered in acoustically injured mice. The animals who received the injury and treatment displayed an increased hair cell number and stimulated hearing recovery. This suggests that γ-secretase inhibition of Notch signaling can be a potential pharmacological therapy in approaching what was previously viewed as permeant deafness. Stem cell therapy
A fetal thymus graft, or rejuvenation of the recipient immunity by inoculation of young CD4+ T cells, also prevents presbycusis as well as up-regulation of the interleukin 1 receptor type II gene (IL1R2) in CD4+ T cells and degeneration of the spiral ganglion in Samp1 mice, a murine model of human senescence. This technology remains years or even decades away from human application.
If the outer hair cells are damaged, they do not regenerate. This results in a loss of sensitivity of hearing, as well as an abnormal perceived loudness in the aspect of the tonotopic spectrum that the damaged cells serve. Neural: characterised by degeneration of cells of the spiral ganglion. Strial/metabolic: characterised by atrophy of stria vascularis in all turns of cochlea. Located in the lateral wall of the cochlea, the stria vascularis contains sodium-potassium-ATPase pumps that are responsible for producing the endolymph resting potential. As individuals age, a loss of capillaries leads to the endolymphatic potential becoming harder to maintain, which brings a decrease in cochlear potential. Cochlear conductive: due to stiffening of the basilar membrane thus affecting its movement. This type of pathology has not been verified as contributing to presbycusis.In addition there are two other types:

Mixed
IndeterminateThe shape of the audiogram categorizes abrupt high-frequency loss (sensory phenotype) or flat loss (strial phenotype). The mainstay of SNHL is strial, with only about 5% of cases being sensory. This type of presbycusis is manifested by a low-frequency hearing loss, with unimpaired speech recognition. Classically, audiograms in neural presbycusis show a moderate downward slope into higher frequencies with a gradual worsening over time. A severe loss in speech discrimination is often described, out of proportion to the threshold loss, making amplification difficult due to poor comprehension.