Tau phosphorylation and cochlear apoptosis cause hearing loss in 3×Tg-AD Mouse Model of Alzheimer's Disease
Clinically typical dementia Alzheimer's disease (AD) is associated with abnormal auditory processing. However, possible molecular mechanisms responsible for the auditory pathology of AD patients are not known. According to our past research findings that the thresholds of auditory brainstem res...
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Medknow Publications
2021-01-01
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| Series: | Chinese Journal of Physiology |
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| Online Access: | http://www.cjphysiology.org/article.asp?issn=0304-4920;year=2021;volume=64;issue=2;spage=61;epage=71;aulast=Wang |
| _version_ | 1819050634056302592 |
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| author | Sheue-Er Wang Chung-Hsin Wu |
| author_facet | Sheue-Er Wang Chung-Hsin Wu |
| author_sort | Sheue-Er Wang |
| collection | DOAJ |
| description | Clinically typical dementia Alzheimer's disease (AD) is associated with abnormal auditory processing. However, possible molecular mechanisms responsible for the auditory pathology of AD patients are not known. According to our past research findings that the thresholds of auditory brainstem response, but not distortion product otoacoustic emissions, were significantly increased in AD mice from 9 months of age and thereafter. Thus, we further explored the possible mechanism of auditory degradation of 3×Tg-AD mice in this study. Our histochemical staining evidence showed the cochlear spiral ganglion neurons (SGN), but not the cochlear hair cells, were lost significantly in the cochlea of 3×Tg-AD mice from 9 months of age and thereafter. Our immunostaining and western blotting evidence showed that phosphorylated tau protein (p-Tau), p-glycogen synthase kinase 3, neurofilament, and apoptosis-related p53, Bcl2-associated X protein, cytochrome c, caspase-9, and caspase-3 were gradually increased, but B-cell lymphoma 2 was gradually decreased with age growth in the cochlea of 3×Tg-AD mice. We suggested that tau hyperphosphorylation and p-Tau 181 aggregation, and mitochondria- and endoplasmic reticulum stress-mediated apoptosis may play a role in the degeneration of SGN in the cochlea. Progressive SGN degeneration in the cochlea may contribute to hearing loss of aging 3×Tg-AD mice. |
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| format | Article |
| id | doaj.art-96f8b57eb92e49e7b45e18a64b2cb05b |
| institution | Directory Open Access Journal |
| issn | 0304-4920 2666-0059 |
| language | English |
| last_indexed | 2024-12-21T11:51:09Z |
| publishDate | 2021-01-01 |
| publisher | Wolters Kluwer Medknow Publications |
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| series | Chinese Journal of Physiology |
| spelling | doaj.art-96f8b57eb92e49e7b45e18a64b2cb05b2022-12-21T19:05:03ZengWolters Kluwer Medknow PublicationsChinese Journal of Physiology0304-49202666-00592021-01-01642617110.4103/CJP.CJP_79_20Tau phosphorylation and cochlear apoptosis cause hearing loss in 3×Tg-AD Mouse Model of Alzheimer's DiseaseSheue-Er WangChung-Hsin WuClinically typical dementia Alzheimer's disease (AD) is associated with abnormal auditory processing. However, possible molecular mechanisms responsible for the auditory pathology of AD patients are not known. According to our past research findings that the thresholds of auditory brainstem response, but not distortion product otoacoustic emissions, were significantly increased in AD mice from 9 months of age and thereafter. Thus, we further explored the possible mechanism of auditory degradation of 3×Tg-AD mice in this study. Our histochemical staining evidence showed the cochlear spiral ganglion neurons (SGN), but not the cochlear hair cells, were lost significantly in the cochlea of 3×Tg-AD mice from 9 months of age and thereafter. Our immunostaining and western blotting evidence showed that phosphorylated tau protein (p-Tau), p-glycogen synthase kinase 3, neurofilament, and apoptosis-related p53, Bcl2-associated X protein, cytochrome c, caspase-9, and caspase-3 were gradually increased, but B-cell lymphoma 2 was gradually decreased with age growth in the cochlea of 3×Tg-AD mice. We suggested that tau hyperphosphorylation and p-Tau 181 aggregation, and mitochondria- and endoplasmic reticulum stress-mediated apoptosis may play a role in the degeneration of SGN in the cochlea. Progressive SGN degeneration in the cochlea may contribute to hearing loss of aging 3×Tg-AD mice.http://www.cjphysiology.org/article.asp?issn=0304-4920;year=2021;volume=64;issue=2;spage=61;epage=71;aulast=Wangalzheimer's diseaseapoptosisauditory brainstem responsecochlear pathologyhearing lossneurofilamentspiral ganglion neuronstau hyperphosphorylationtransgenic mice |
| spellingShingle | Sheue-Er Wang Chung-Hsin Wu Tau phosphorylation and cochlear apoptosis cause hearing loss in 3×Tg-AD Mouse Model of Alzheimer's Disease Chinese Journal of Physiology alzheimer's disease apoptosis auditory brainstem response cochlear pathology hearing loss neurofilament spiral ganglion neurons tau hyperphosphorylation transgenic mice |
| title | Tau phosphorylation and cochlear apoptosis cause hearing loss in 3×Tg-AD Mouse Model of Alzheimer's Disease |
| title_full | Tau phosphorylation and cochlear apoptosis cause hearing loss in 3×Tg-AD Mouse Model of Alzheimer's Disease |
| title_fullStr | Tau phosphorylation and cochlear apoptosis cause hearing loss in 3×Tg-AD Mouse Model of Alzheimer's Disease |
| title_full_unstemmed | Tau phosphorylation and cochlear apoptosis cause hearing loss in 3×Tg-AD Mouse Model of Alzheimer's Disease |
| title_short | Tau phosphorylation and cochlear apoptosis cause hearing loss in 3×Tg-AD Mouse Model of Alzheimer's Disease |
| title_sort | tau phosphorylation and cochlear apoptosis cause hearing loss in 3 tg ad mouse model of alzheimer s disease |
| topic | alzheimer's disease apoptosis auditory brainstem response cochlear pathology hearing loss neurofilament spiral ganglion neurons tau hyperphosphorylation transgenic mice |
| url | http://www.cjphysiology.org/article.asp?issn=0304-4920;year=2021;volume=64;issue=2;spage=61;epage=71;aulast=Wang |
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