Molecular pathogenesis and disease-modifying therapies of Alzheimer's disease and related disorders
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DOI[10.31662/jmaj.2022-0079]to the data of the same series
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- Material Type
- 記事
- Title
- Author/Editor
- Takeshi Iwatsubo
- Publication, Distribution, etc.
- Publication Date
- 2022-07-15
- Publication Date (W3CDTF)
- 2022-07-15
- Periodical title
- JMA Journal
- No. or year of volume/issue
- 5(3)
- Volume
- 5(3)
- ISSN (Periodical Title)
- 2433-3298
- ISSN-L (Periodical Title)
- 2433-328X
- Text Language Code
- eng
- DOI
- 10.31662/jmaj.2022-0079
- Persistent ID (NDL)
- info:ndljp/pid/14494927
- Collection
- Collection (Materials For Handicapped People:1)
- Collection (particular)
- 国立国会図書館デジタルコレクション > 電子書籍・電子雑誌 > その他
- Acquisition Basis
- インターネット資料収集保存事業（WARP）
- Date Accepted (W3CDTF)
- 2025-10-21T09:04:40+09:00
- Date Captured (W3CDTF)
- 2024-09-26
- Format (IMT)
- application/pdf
- Access Restrictions
- インターネット公開
- Availability of remote photoduplication service
- 不可
- Periodical Title (URI)
- Periodical Title (Persistent ID (NDL))
- info:ndljp/pid/14494924
- Data Provider (Database)
- 国立国会図書館 : 国立国会図書館デジタルコレクション
- Summary, etc.
- <p>The deposition of amyloid β (Aβ) peptides as senile plaques and tau as neurofibrillary changes causes the hallmark neuropathological lesions of Alzheimer's disease (AD), which are implicated in its pathogenesis and deemed as the prime target for disease-modifying therapies (DMTs). Aβ is produced by sequential proteolytic cleavage by β- and γ-secretases. γ-Secretase, harboring presenilins (PS) as the catalytic center, forms the C-terminus of Aβ that determines its propensity to aggregate; missense mutations in PS genes cause familial AD by altering the preferred γ-secretase cleavage sites to increase the production of pathogenic Aβ42 species. Numerous DMTs for AD have been tested in clinical trials, some of which met the clinical endpoints, whereas others, especially those conducted in dementia stages, have failed, underscoring the needs for early intervention. Notably, positive outcomes of recent trials for anti-Aβ antibody drugs have depended largely on molecular imaging and fluid biomarkers, underscoring the needs of markers that surrogate the clinical and pathophysiological progression of AD. Longitudinal observational studies as represented by the AD Neuroimaging Initiative (ADNI) in North America, as well as the Japanese ADNI (J-ADNI), have contributed greatly toward the goal of very early treatment at the prodromal and preclinical AD stages by delineating the early natural course of AD and facilitating the development of biomarkers. It has been demonstrated that the clinical and biomarker profiles of prodromal AD in J-ADNI were remarkably similar to those in the North American ADNI, supporting the harmonization of global clinical trials. These clinical studies in Japan, accelerated by the development and implementation of biomarkers, will pave the way toward the development of AD therapies targeting its very early stages.</p>
- DOI
- 10.31662/jmaj.2022-0079
- Access Restrictions
- インターネット公開
- Data Provider (Database)
- 科学技術振興機構 : J-STAGE
- Summary, etc.
- <p>The deposition of amyloid β (Aβ) peptides as senile plaques and tau as neurofibrillary changes causes the hallmark neuropathological lesions of Alzheimer's disease (AD), which are implicated in its pathogenesis and deemed as the prime target for disease-modifying therapies (DMTs). Aβ is produced by sequential proteolytic cleavage by β- and γ-secretases. γ-Secretase, harboring presenilins (PS) as the catalytic center, forms the C-terminus of Aβ that determines its propensity to aggregate; missense mutations in PS genes cause familial AD by altering the preferred γ-secretase cleavage sites to increase the production of pathogenic Aβ42 species. Numerous DMTs for AD have been tested in clinical trials, some of which met the clinical endpoints, whereas others, especially those conducted in dementia stages, have failed, underscoring the needs for early intervention. Notably, positive outcomes of recent trials for anti-Aβ antibody drugs have depended largely on molecular imaging and fluid biomarkers, underscoring the needs of markers that surrogate the clinical and pathophysiological progression of AD. Longitudinal observational studies as represented by the AD Neuroimaging Initiative (ADNI) in North America, as well as the Japanese ADNI (J-ADNI), have contributed greatly toward the goal of very early treatment at the prodromal and preclinical AD stages by delineating the early natural course of AD and facilitating the development of biomarkers. It has been demonstrated that the clinical and biomarker profiles of prodromal AD in J-ADNI were remarkably similar to those in the North American ADNI, supporting the harmonization of global clinical trials. These clinical studies in Japan, accelerated by the development and implementation of biomarkers, will pave the way toward the development of AD therapies targeting its very early stages.</p>
- DOI
- 10.31662/jmaj.2022-0079
- Related Material (URI)
- Data Provider (Database)
- 国立情報学研究所 : CiNii Research
- Original Data Provider (Database)
- Japan Link Center雑誌記事索引データベースCrossref科学研究費助成事業データベース
- Bibliographic ID (NDL)
- 14494927