It is known that CX3C chemokine receptor 1 (CX3CR1) expressed on macrophages plays a crucial role in inner hair cell ribbon synaptic repair and spiral ganglion neuron survival after synaptopathic noise-induced trauma.
The most common genetic cause of hereditary deafness in humans are mutations in the GJB2 gene, especially the 35delG and 235delC mutations. At the recent ARO meeting, researchers from Ear Nose and Throat Hospital of Fudan University presented the creation of a novel mouse model for studying the pathogenic mechanisms of hereditary deafness resulting from these mutations.
Noise-induced hearing loss is still the most common cause of acquired hearing loss nowadays. The mechanisms behind this may be explained through inflammatory responses in the cochlea after acoustic trauma.
It has been previously demonstrated that noise exposure leads to activation of the mitogen-activated protein kinase (MAPK) pathway, and that inhibition of this pathway protects from hearing loss. Tizaterkib (formerly AZD-0364) is a novel, highly selective, orally bioavailable ERK1/2 inhibitor that is currently in early clinical development for the treatment of cancer. In recent work, investigators from Creighton University aimed to assess the potential of tizaterkib for the treatment of noise-induced hearing loss (NIHL).
Takara Bio Inc. has announced the development of a novel adeno-associated virus (AAV) vector, Sonuaav, which exhibits high gene transfer efficiency into inner ear tissues, with a collaborator at Juntendo University School of Medicine.
Researchers from the University of Copenhagen, Karolinska Institutet and affiliated organizations have reported the discovery of a novel gene therapy delivered through a cerebrospinal fluid (CSF) conduit as new treatment strategy for hearing loss.