TY - JOUR
T1 - Age-related loss of spiral ganglion neurons
AU - Bao, Jianxin
AU - Ohlemiller, Kevin K.
N1 - Funding Information:
We would like thank Ms. Joyce Ji for comments on the manuscript. Supported by the National Organization for Hearing Research Foundation (J.B.), NIH R21 DC010489 (J.B.), NIH R01 AG024250 (J.B.), R01 DC008321 (K.K.O.), and P30 DC04665 (R. Chole).
PY - 2010/6
Y1 - 2010/6
N2 - Spiral ganglion neurons (SGNs) are the relay station for auditory information between hair cells and central nervous system. Age-related decline of auditory function due to SGN loss can not be ameliorated by hearing aids or cochlear implants. Recent findings clearly indicate that survival of SGNs during aging depends on genetic and environmental interactions, which can be demonstrated at the systemic, tissue, cellular, and molecular levels. At the systemic level, both insulin/insulin-like growth factor-1 and lipophilic/steroid hormone pathways influence SGN survival during aging. At the level of organ of the Corti, it is difficult to determine whether age-related SGN loss is primary or secondary degeneration. However, a late stage of SGN degeneration may be independent of age-related loss of hair cells. At the cellular and molecular level, several pathways, particularly free radical and calcium signaling pathways, can influence age-related SGN loss, and further studies should determine how these pathways contribute to SGN loss, such as whether they directly or indirectly act on SGNs. With the advancement of recent genetic and pharmacologic tools, we should not only understand how SGNs die during aging, but also find ways to delay this loss.
AB - Spiral ganglion neurons (SGNs) are the relay station for auditory information between hair cells and central nervous system. Age-related decline of auditory function due to SGN loss can not be ameliorated by hearing aids or cochlear implants. Recent findings clearly indicate that survival of SGNs during aging depends on genetic and environmental interactions, which can be demonstrated at the systemic, tissue, cellular, and molecular levels. At the systemic level, both insulin/insulin-like growth factor-1 and lipophilic/steroid hormone pathways influence SGN survival during aging. At the level of organ of the Corti, it is difficult to determine whether age-related SGN loss is primary or secondary degeneration. However, a late stage of SGN degeneration may be independent of age-related loss of hair cells. At the cellular and molecular level, several pathways, particularly free radical and calcium signaling pathways, can influence age-related SGN loss, and further studies should determine how these pathways contribute to SGN loss, such as whether they directly or indirectly act on SGNs. With the advancement of recent genetic and pharmacologic tools, we should not only understand how SGNs die during aging, but also find ways to delay this loss.
KW - Aging
KW - Calcium
KW - Caloric restriction
KW - Glucocorticoid
KW - Hair cell
KW - Neural presbycusis
KW - Spiral ganglion neuron
UR - http://www.scopus.com/inward/record.url?scp=77952674056&partnerID=8YFLogxK
U2 - 10.1016/j.heares.2009.10.009
DO - 10.1016/j.heares.2009.10.009
M3 - Article
C2 - 19854255
AN - SCOPUS:77952674056
SN - 0378-5955
VL - 264
SP - 93
EP - 97
JO - Hearing research
JF - Hearing research
IS - 1-2
ER -