The TRPM2 channel nexus from oxidative damage to Alzheimers pathologies: an emerging novel intervention target for age-related dementia
Alzheimer's disease (AD), an age-related neurodegenerative condition, is the most common cause of dementia among the elder people, but currently there is no treatment. A number of putative pathogenic events, particularly amyloid β peptide (Aβ) accumulation, are believed to be early triggers tha...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2018
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| Online Access: | http://psasir.upm.edu.my/id/eprint/74277/1/The%20TRPM2%20channel%20nexus%20from%20oxidative%20damage%20to%20Alzheimers%20pathologies.pdf |
| _version_ | 1796979702609477632 |
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| author | Jiang, Lin-Hua Li, Xin Syed Mortadza, Sharifah Alawieyah Lovatt, Megan Yang, Wei |
| author_facet | Jiang, Lin-Hua Li, Xin Syed Mortadza, Sharifah Alawieyah Lovatt, Megan Yang, Wei |
| author_sort | Jiang, Lin-Hua |
| collection | UPM |
| description | Alzheimer's disease (AD), an age-related neurodegenerative condition, is the most common cause of dementia among the elder people, but currently there is no treatment. A number of putative pathogenic events, particularly amyloid β peptide (Aβ) accumulation, are believed to be early triggers that initiate AD. However, thus far targeting Aβ generation/aggregation as the mainstay strategy of drug development has not led to effective AD-modifying therapeutics. Oxidative damage is a conspicuous feature of AD, but this remains poorly defined phenomenon and mechanistically ill understood. The TRPM2 channel has emerged as a potentially ubiquitous molecular mechanism mediating oxidative damage and thus plays a vital role in the pathogenesis and progression of diverse neurodegenerative diseases. This article will review the emerging evidence from recent studies and propose a novel 'hypothesis' that multiple TRPM2-mediated cellular and molecular mechanisms cascade Aβ and/or oxidative damage to AD pathologies. The 'hypothesis' based on these new findings discusses the prospect of considering the TRPM2 channel as a novel therapeutic target for intervening AD and age-related dementia. |
| first_indexed | 2024-03-06T10:12:47Z |
| format | Article |
| id | upm.eprints-74277 |
| institution | Universiti Putra Malaysia |
| language | English |
| last_indexed | 2024-03-06T10:12:47Z |
| publishDate | 2018 |
| publisher | Elsevier |
| record_format | dspace |
| spelling | upm.eprints-742772020-04-02T07:53:51Z http://psasir.upm.edu.my/id/eprint/74277/ The TRPM2 channel nexus from oxidative damage to Alzheimers pathologies: an emerging novel intervention target for age-related dementia Jiang, Lin-Hua Li, Xin Syed Mortadza, Sharifah Alawieyah Lovatt, Megan Yang, Wei Alzheimer's disease (AD), an age-related neurodegenerative condition, is the most common cause of dementia among the elder people, but currently there is no treatment. A number of putative pathogenic events, particularly amyloid β peptide (Aβ) accumulation, are believed to be early triggers that initiate AD. However, thus far targeting Aβ generation/aggregation as the mainstay strategy of drug development has not led to effective AD-modifying therapeutics. Oxidative damage is a conspicuous feature of AD, but this remains poorly defined phenomenon and mechanistically ill understood. The TRPM2 channel has emerged as a potentially ubiquitous molecular mechanism mediating oxidative damage and thus plays a vital role in the pathogenesis and progression of diverse neurodegenerative diseases. This article will review the emerging evidence from recent studies and propose a novel 'hypothesis' that multiple TRPM2-mediated cellular and molecular mechanisms cascade Aβ and/or oxidative damage to AD pathologies. The 'hypothesis' based on these new findings discusses the prospect of considering the TRPM2 channel as a novel therapeutic target for intervening AD and age-related dementia. Elsevier 2018 Article PeerReviewed text en http://psasir.upm.edu.my/id/eprint/74277/1/The%20TRPM2%20channel%20nexus%20from%20oxidative%20damage%20to%20Alzheimers%20pathologies.pdf Jiang, Lin-Hua and Li, Xin and Syed Mortadza, Sharifah Alawieyah and Lovatt, Megan and Yang, Wei (2018) The TRPM2 channel nexus from oxidative damage to Alzheimers pathologies: an emerging novel intervention target for age-related dementia. Ageing Research Reviews, 47. 67 - 79. ISSN 1568-1637; EISSN: 1872-9649 10.1016/j.arr.2018.07.002 |
| spellingShingle | Jiang, Lin-Hua Li, Xin Syed Mortadza, Sharifah Alawieyah Lovatt, Megan Yang, Wei The TRPM2 channel nexus from oxidative damage to Alzheimers pathologies: an emerging novel intervention target for age-related dementia |
| title | The TRPM2 channel nexus from oxidative damage to Alzheimers pathologies: an emerging novel intervention target for age-related dementia |
| title_full | The TRPM2 channel nexus from oxidative damage to Alzheimers pathologies: an emerging novel intervention target for age-related dementia |
| title_fullStr | The TRPM2 channel nexus from oxidative damage to Alzheimers pathologies: an emerging novel intervention target for age-related dementia |
| title_full_unstemmed | The TRPM2 channel nexus from oxidative damage to Alzheimers pathologies: an emerging novel intervention target for age-related dementia |
| title_short | The TRPM2 channel nexus from oxidative damage to Alzheimers pathologies: an emerging novel intervention target for age-related dementia |
| title_sort | trpm2 channel nexus from oxidative damage to alzheimers pathologies an emerging novel intervention target for age related dementia |
| url | http://psasir.upm.edu.my/id/eprint/74277/1/The%20TRPM2%20channel%20nexus%20from%20oxidative%20damage%20to%20Alzheimers%20pathologies.pdf |
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