Drug candidates in clinical trials for Alzheimer’s disease
Open accessAbstract
Alzheimer’s disease (AD) is a major form of senile dementia, characterized by progressive memory and neuronal loss combined with cognitive impairment. AD is the most common neurodegenerative disease worldwide, affecting one-fifth of those aged over 85 years. Recent therapeutic approaches have been strongly influenced by five neuropathological hallmarks of AD: acetylcholine deficiency, glutamate excitotoxicity, extracellular deposition of amyloid-β (Aβ plague), formation of intraneuronal neurofibrillary tangles (NTFs), and neuroinflammation. The lowered concentrations of acetylcholine (ACh) in AD result in a progressive and significant loss of cognitive and behavioral function. Current AD medications, memantine and acetylcholinesterase inhibitors (AChEIs) alleviate some of these symptoms by enhancing cholinergic signaling, but they are not curative. Since 2003, no new drugs have been approved for the treatment of AD. This article focuses on the current research in clinical trials targeting the neuropathological findings of AD including acetylcholine response, glutamate transmission, Aβ clearance, tau protein deposits, and neuroinflammation. These investigations include acetylcholinesterase inhibitors, agonists and antagonists of neurotransmitter receptors, β-secretase (BACE) or γ-secretase inhibitors, vaccines or antibodies targeting Aβ clearance or tau protein, as well as anti-inflammation compounds. Ongoing Phase III clinical trials via passive immunotherapy against Aβ peptides (crenezumab, gantenerumab, and aducanumab) seem to be promising. Using small molecules blocking 5-HT 6 serotonin receptor (intepirdine), inhibiting BACE activity (E2609, AZD3293, and verubecestat), or reducing tau aggregation (TRx0237) are also currently in Phase III clinical trials. We here systemically review the findings from recent clinical trials to provide a comprehensive review of novel therapeutic compounds in the treatment and prevention of AD.
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Currently approved drugs do little to limit Alzheimer's disease progression, and no preventive therapies are available.
“Currently approved drugs do little to limit disease progression, and no preventive therapies are available.3,4”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [4]
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- Authors
- Hung, S.-Y., & Fu, W.-M.
- Affiliations
- China Medical University (TW)
- National Taiwan University (TW)
- Corresponding author
- Fu, Wen-Mei
- Venue
- Journal of Biomedical Science
- Published
- 2017-07-19
- Volume
- 24
- Issue
- 1
- Pages
- 47-47
- ISSN
- 1021-7770 (ISSN-L)
- 1423-0127
- PMC
- PMC5516350
- OpenAlex
- W2737900099
- Cited by
- 420
- References
- 72
- Citations by year
- 2026: 14 · 2025: 26 · 2024: 39 · 2023: 48 · 2022: 54 · 2021: 48 · 2020: 54 · 2019: 59 · 2018: 67 · 2017: 10
- FWCI
- 6.37
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by
- Locations
- Journal of Biomedical Science (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Ministry of Science and Technology, Taiwan (MOST 105-2320-B-039-009-)
- China Medical University, Taiwan (CMU104-N-10)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Pharmacology › Cholinesterase and Neurodegenerative Diseases
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, drug candidates, clinical trials, acetylcholinesterase inhibitors, memantine, acetylcholine deficiency, glutamate excitotoxicity, amyloid-beta clearance, tau protein, neuroinflammation, BACE inhibitors, gamma-secretase inhibitors, anti-amyloid antibodies, passive immunotherapy, serotonin 5-HT6 receptor, neurodegeneration
- MeSH terms
- Alzheimer Disease, Antibodies, Monoclonal, Clinical Trials as Topic, Immunotherapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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