Cited by 105Alzheimer's disease research and treatmentsCholinesterase and Neurodegenerative DiseasesDementia and Cognitive Impairment Research

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New therapeutics beyond amyloid-β and tau for the treatment of Alzheimer’s disease

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Zhang, Feng, Zhong, Ru-jia, Cheng, Cheng, Li, Song, Le, Wei-dong·2021·Acta Pharmacologica Sinica

DOI 10.1038/s41401-020-00565-5PMC PMC8379190

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Abstract

As the population ages, Alzheimer's disease (AD), the most common neurodegenerative disease in elderly people, will impose social and economic burdens to the world. Currently approved drugs for the treatment of AD including cholinesterase inhibitors (donepezil, rivastigmine, and galantamine) and an N-methyl-D-aspartic acid receptor antagonist (memantine) are symptomatic but poorly affect the progression of the disease. In recent decades, the concept of amyloid-β (Aβ) cascade and tau hyperphosphorylation leading to AD has dominated AD drug development. However, pharmacotherapies targeting Aβ and tau have limited success. It is generally believed that AD is caused by multiple pathological processes resulting from Aβ abnormality, tau phosphorylation, neuroinflammation, neurotransmitter dysregulation, and oxidative stress. In this review we updated the recent development of new therapeutics that regulate neurotransmitters, inflammation, lipid metabolism, autophagy, microbiota, circadian rhythm, and disease-modified genes for AD in preclinical research and clinical trials. It is to emphasize the importance of early diagnosis and multiple-target intervention, which may provide a promising outcome for AD treatment.

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“Amyloid-β (Aβ)-targeted immunotherapies and β-secretase (BACE1) inhibitors such as AN-1792 [3], bapineuzumab [4], solanezumab [5], aducanumab [6], gantenerumab [7], verubecestat [8], atabecestat [9], lanabecestat [10], and elenbecestat (E2609) [11] have shown a lack of efficacy in improving cognition in AD patients.”
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Additional file 4 of Associations of MRI-visible perivascular spaces with longitudinal cognitive decline across the Alzheimer’s disease spectrum
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Additional file 2 of Associations of MRI-visible perivascular spaces with longitudinal cognitive decline across the Alzheimer’s disease spectrum
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Additional file 1 of Associations of MRI-visible perivascular spaces with longitudinal cognitive decline across the Alzheimer’s disease spectrum
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Additional file 5 of Associations of MRI-visible perivascular spaces with longitudinal cognitive decline across the Alzheimer’s disease spectrum
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Additional file 7 of Associations of MRI-visible perivascular spaces with longitudinal cognitive decline across the Alzheimer’s disease spectrum
Wang, M.-L., Zou, Q.-Q., Sun, Z., Wei, X.-E., Li, P., Wu, X., & Li, Y.-H. (2023) · Figshare · doi:10.6084/m9.figshare.22600112
Additional file 6 of Associations of MRI-visible perivascular spaces with longitudinal cognitive decline across the Alzheimer’s disease spectrum
Wang, M.-L., Zou, Q.-Q., Sun, Z., Wei, X.-E., Li, P., Wu, X., & Li, Y.-H. (2023) · Figshare · doi:10.6084/m9.figshare.22600109
Additional file 9 of Associations of MRI-visible perivascular spaces with longitudinal cognitive decline across the Alzheimer’s disease spectrum
Wang, M.-L., Zou, Q.-Q., Sun, Z., Wei, X.-E., Li, P., Wu, X., & Li, Y.-H. (2023) · Figshare · doi:10.6084/m9.figshare.22600118
Additional file 8 of Associations of MRI-visible perivascular spaces with longitudinal cognitive decline across the Alzheimer’s disease spectrum
Wang, M.-L., Zou, Q.-Q., Sun, Z., Wei, X.-E., Li, P., Wu, X., & Li, Y. (2023) · Figshare · doi:10.6084/m9.figshare.22600115
Additional file 3 of Associations of MRI-visible perivascular spaces with longitudinal cognitive decline across the Alzheimer’s disease spectrum
Wang, M.-L., Zou, Q.-Q., Sun, Z., Wei, X.-E., Li, P.-Y., Wu, X., & Li, Y.-H. (2023) · Figshare · doi:10.6084/m9.figshare.22600100
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Implication physio-pathologique de l'axe de signalisation PrPC-ADAM10/17 : des maladies neurodégénératives aux cancers
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Authors: Zhang, F., Zhong, R.-J., Cheng, C., Li, S., & Le, W.-D.
Affiliations: Dalian Medical University (CN)
ORCID: Zhang, Feng
Cheng, Cheng
Li, Song
Venue: Acta Pharmacologica Sinica
Publisher: Springer Science and Business Media LLC
Published: 2020-12-02
Volume: 42
Issue: 9
Pages: 1382-1389
ISSN: 0253-9756 (ISSN-L)
1671-4083
1745-7254
DOI: 10.1038/s41401-020-00565-5
PMC: PMC8379190
OpenAlex: W3106951507
Cited by: 105
References: 118
Citations by year: 2026: 9 · 2025: 16 · 2024: 21 · 2023: 32 · 2022: 15 · 2021: 12
FWCI: 1.88
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Acta Pharmacologica Sinica (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Natural Science Foundation of China (81771521)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Pharmacology (medical) › Cholinesterase and Neurodegenerative Diseases
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: Alzheimer's disease, amyloid-beta, tau hyperphosphorylation, disease-modifying therapy, neuroinflammation, neurotransmitter dysregulation, oxidative stress, lipid metabolism, autophagy, gut microbiota, circadian rhythm, early diagnosis, cholinesterase inhibitors, memantine, preclinical drug development
MeSH terms: Neuroinflammatory Diseases, Aged, Alzheimer Disease, Cholinesterase Inhibitors, Humans, Phosphorylation, Amyloid beta-Peptides, tau Proteins, Neurodegenerative Diseases

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New therapeutics beyond amyloid-β and tau for the treatment of Alzheimer’s disease

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