Theoretical and Natural Science

- The Open Access Proceedings Series for Conferences

Theoretical and Natural Science

Vol. 6, 03 August 2023

Open Access | Article

A review of current developments in Alzheimer’s disease treatment methods

Linfeng Xu * 1
1 Hangzhou Medical College

* Author to whom correspondence should be addressed.

Theoretical and Natural Science, Vol. 6, 29-34
Published 03 August 2023. © 2023 The Author(s). Published by EWA Publishing
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Citation Linfeng Xu. A review of current developments in Alzheimer’s disease treatment methods. TNS (2023) Vol. 6: 29-34. DOI: 10.54254/2753-8818/6/20230126.


This article will summarize the results of recent years of exploration into deeper causes of Alzheimer’s disease with possible therapeutic strategies. The most popular pathological hypothesis for the causation of Alzheimer’s is the Aβ cascade hypothesis. Aβ has a dominant role in the pathophysiology of Alzheimer’s disease, according to genetic and pathological data. Another significant histological characteristic of Alzheimer’s disease brains is the presence of neurofibrillary tangles made of the protein tau, which is related with microtubules. In the brain, neuronal loss, neuroinflammation, and oxidative stress can result from the cascade consequences of tau toxicity. But as research has progressed, it has been found the Aβ. The accumulation of protein and neurofibrillary tangles composed of phosphorylated tau are only manifestations of AD, not the result. This is also the reason why many drugs fail the phase III clinic. So people began to look for a way out of the problem, starting in the direction of the gene. How to diagnose AD early in the MCI stage, how to find markers for early diagnosis and how to inhibit the progression from the MCI stage to the dementia stage are all questions that need to be investigated in the future.


AD, tau Aβ, ApoE, gene, review treatment


1. Nakamura, T., Oh, C. K., Liao, L., Zhang, X., Lopez, K. M., Gibbs, D., ... & Lipton, S. A. Noncanonical transnitrosylation network contributes to synapse loss in Alzheimer’s disease. Science, 371(6526), eaaw0843. (2021).

2. Lecanemab Confirmatory Phase 3 Clarity AD Study Met Primary Endpoint, Showing Highly Statistically Significant Reduction of Clinical Decline in Large Global Clinical Study of 1,795 Paticipants with Early Alzheimer’s disease.

3. Swanson, C. J., Zhang, Y., Dhadda, S., Wang, J., Kaplow, J., Lai, R. Y., ... & Cummings, J. L. A randomized, double-blind, phase 2b proof-of-concept clinical trial in early Alzheimer’s disease with lecanemab, an anti-Aβ protofibril antibody. Alzheimer’s research & therapy, 13(1), 1-14. (2021).

4. The U.S. Food and Drug Administration. FDA’sDecision to Approve New Treatment for Alzheimer’s Disease [EB/OL]. [2021-06-07]

5. Lee JH, Yang DS, Goulbourne CN, Im E, Stavrides P, Pensalfini A, Chan H, Bouchet-Marquis C, Bleiwas C, Berg MJ, Huo C, Peddy J, Pawlik M, Levy E, Rao M, Staufenbiel M, Nixon RA. Faulty autolysosome acidification in Alzheimer’s disease mouse models induces autophagic build-up of Aβ in neurons, yielding senile plaques. Nat Neurosci. 25(6):688-701. 2022 Jun. doi: 10.1038/s41593-022-01084-8. Epub 2022 Jun 2. PMID: 35654956; PMCID: PMC9174056.

6. Liu E, Schmidt M E, Margolin R, et al. Amyloid-β 11C-PiB-PET imaging results from 2 randomized bapineuzumab phase 3 AD trials[J]. Neurology, 85(8):692-700. 2015.

7. Busche M A , Hyman B T . Synergy between amyloid-β and tau in Alzheimer's disease[J]. Nature Neuroscience.

8. Hosokawa M , Arai T , Masuda-Suzukake M , et al. Methylene Blue Reduced Abnormal Tau Accumulation in P301L Tau Transgenic Mice[J]. Plos One, 2012, 7(12):e52389.

9. Schaler AW, Runyan AM, Clelland CL, Sydney EJ, Fowler SL, Figueroa HY, Shioda S, Santa-Maria I, Duff KE, Myeku N. PAC1 receptor-mediated clearance of tau in postsynaptic compartments attenuates tau pathology in mouse brain. Sci Transl Med. 13(595):eaba7394. 2021 May 26. doi: 10.1126/scitranslmed.aba7394. PMID: 34039738; PMCID: PMC8988215.

10. Hung SY, Fu WM. Drug candidates in clinical trials for Alzheimer’s disease. J Biomed Sci. 24(1):47. 2017 Jul 19. doi: 10.1186/s12929-017-0355-7. PMID: 28720101; PMCID: PMC5516350.

11. Huang Y, Mucke L. Alzheimer Mechanisms and Therapeutic Strategies[J]. CELL-CAMBRIDGE MA-, 148(6):1204-1222. 2012.

12. Najm R, Jones E A, Huang Y. Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease[J]. Molecular Neurodegeneration, 14(1). 2019.

13. Wang, C. et al. Gain of toxic apolipoprotein E4 effects in human iPSC-derived neurons is ameliorated by a small-molecule structure corrector. Nat. Med. 24, 647–657 (2018).

14. Xu, Q., Bernardo, A., Walker, D., Kanegawa, T., Mahley, R. W., & Huang, Y. Profile and regulation of apolipoprotein E (ApoE) expression in the CNS in mice with targeting of green fluorescent protein gene to the ApoE locus. Journal of Neuroscience, 26(19), 4985-4994. (2006).

15. Lin, Y.-T. et al. APOE4 causes widespread molecular and cellular alterations associated with Alzheimer’s disease phenotypes in human iPSC-derived brain cell types. Neuron 98, 1141–1154. (2018).

16. Zalocusky, K. A., Najm, R., Taubes, A. L., Hao, Y., Yoon, S. Y., Koutsodendris, N., ... & Huang, Y. Neuronal ApoE upregulates MHC-I expression to drive selective neurodegeneration in Alzheimer’s disease. Nature Neuroscience, 24(6), 786-798. (2021).

17. First-in-human clinical trial to assess gene therapy for Alzheimer’s disease.

18. Tremblay G, Rousseau J, Mbakam CH, Tremblay JP. Insertion of the Icelandic Mutation (A673T) by Prime Editing: A Potential Preventive Treatment for Familial and Sporadic Alzheimer’s Disease. CRISPR J. 5(1):109-122. (2022). doi:10.1089/crispr.2021.0085

19. Mishra, R., Phan, T., Kumar, P., Morrissey, Z., Gupta, M., Hollands, C., ... & Lazarov, O. Augmenting neurogenesis rescues memory impairments in Alzheimer’s disease by restoring the memory-storing neurons. Journal of Experimental Medicine, 219(9). (2022).

Data Availability

The datasets used and/or analyzed during the current study will be available from the authors upon reasonable request.

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Volume Title
Proceedings of the International Conference on Modern Medicine and Global Health (ICMMGH 2023)
ISBN (Print)
ISBN (Online)
Published Date
03 August 2023
Theoretical and Natural Science
ISSN (Print)
ISSN (Online)
03 August 2023
Open Access
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

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