Disease relevance of Presbycusis

• Of the 88 patients with hearing loss, 63 (71.6%) had sensorineural, 20 (22.7%) had presbycusis, 1 (1.1%) had conductive, and 4 (4.6%) had mixed hearing loss [1].
• A patient is described illustrating some of these factors, in which exposure to noise, head injury, ototoxic drug ingestion, childhood ear disease, otosclerosis, and presbycusis compounded to create a clinical conundrum [2].
• In a cohort of unrelated patients with Meniere's Disease, otosclerosis and strial presbycusis as well as other types of sensorineural hearing losses, we have identified an extended MHC haplotype common to the majority of these patients, supporting a hypothesis that a gene(s) within the MHC domain may confer susceptibility to these hearing ailments [3].

Psychiatry related information on Presbycusis

• This article suggests a working definition of "classic presbycusis," which may be defined as a syndrome involving (1) a bilaterally symmetric sensorineural hearing loss, (2) absent or partial recruitment, (3) negative noise history, and (4) poorer speech discrimination than indicated by pure tones (phonemic regression) [4].

High impact information on Presbycusis

• These findings represent VPA-induced sensorineural hearing loss, possibly in preexisting presbycusis [5].
• Presbycusis may result, in part, from functional loss of the inhibitory neurotransmitter GABA [6].
• Aging and presbycusis: effects on 2-deoxy-D-glucose uptake in the mouse auditory brain stem in quiet [7].
• Prednisolone administration showed no significant prevention of the development of presbycusis in the mice, suggesting that autoimmune mechanisms are not involved in the acceleration of presbycusis [8].
• Higher serum aldosterone correlates with lower hearing thresholds: a possible protective hormone against presbycusis [9].

Chemical compound and disease context of Presbycusis

• Metabolic presbycusis: differential changes in auditory brainstem and otoacoustic emission responses with chronic furosemide application in the gerbil [10].
• Given the major role glycine plays in normal CN function, changes in glycine-receptor activity may contribute to central presbycusis [11].
• A higher synthesis of DA in aged animals could support these findings, which could indicate some kind of compensatory mechanism related to presbycusis [12].

Biological context of Presbycusis

• Missense mutations in CDH23 have been associated with presbycusis and DFNB12, whereas null alleles cause the majority of Usher 1D [13].
• Also, the combinations of different GSTM1, GSTT1, and GSTP1 genotypes were not an increased risk of presbycusis (p > 0.05) [14].

Gene context of Presbycusis

• RESULTS: Gene polymorphisms at GSTM1, GSTT1, and GSTP1 in subjects with presbycusis were not significantly different than in the controls (p > 0.05) [14].
• The caused by presbycusis, combined with a recurrent conductive loss in the speech frequencies rather than cochlear otosclerosis [15].
• Presbycusis: the aging ear. Part I [16].
• A significantly decreased expression of the beta2 nAChR subunit in SGNs was found specifically in mice susceptible to presbycusis [17].
• This study examines the effects of high intensity noise exposure (0.5-40 kHz noise at 108 dB SPL for 45 min) on young and old normal (CBA/Ca) mice and young premature presbycusis (C57BL/6) mice [18].

References