Evidence map›Paper›PMID 41049735›Full record

ReviewActa pharmaceutica Sinica. B2025

Artificial intelligence in drug development for delirium and Alzheimer's disease.

Ruixue Ai, Xianglu Xiao, Shenglong Deng, Nan Yang, Xiaodan Xing, Leiv Otto Watne, Geir Selbæk, Yehani Wedatilake, Chenglong Xie, David C Rubinsztein and 6 more

Abstract readReview
In one paragraph

Review in Acta pharmaceutica Sinica. B, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Ruixue AiDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog 1478, Norway.
Xianglu XiaoBioengineering Department and Imperial-X, Imperial College London, London W12 7SL, UK.
Shenglong DengBioengineering Department and Imperial-X, Imperial College London, London W12 7SL, UK.
Nan YangBioengineering Department and Imperial-X, Imperial College London, London W12 7SL, UK.
Xiaodan XingBioengineering Department and Imperial-X, Imperial College London, London W12 7SL, UK.
Leiv Otto WatneDepartment of Geriatric Medicine, Akershus University Hospital, Lørenskog 1478, Norway.
Geir SelbækNorwegian National Centre for Ageing and Health, Vestfold Hospital Trust, Tønsberg 3103, Norway.
Yehani WedatilakeNorwegian National Centre for Ageing and Health, Vestfold Hospital Trust, Tønsberg 3103, Norway.
Chenglong XieDepartment of Neurology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
David C RubinszteinCambridge Institute for Medical Research (CIMR), University of Cambridge, Cambridge CB2 0XY, UK.
Jennifer E PalmerCambridge Institute for Medical Research (CIMR), University of Cambridge, Cambridge CB2 0XY, UK.
Bjørn Erik NeerlandDepartment of Geriatric Medicine, Oslo University Hospital, Oslo 0450, Norway.
Hongming ChenGuangzhou National Laboratory, Guangzhou 510005, China.
Zhangming NiuMindrank AI Ltd., Hangzhou 310018, China.
Guang YangBioengineering Department and Imperial-X, Imperial College London, London W12 7SL, UK.
Evandro Fei FangDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog 1478, Norway.

Funding

Wellcome Trust
6 · The paper itself

Abstract

Delirium is a common cause and complication of hospitalization in the elderly and is associated with higher risk of future dementia and progression of existing dementia, of which 70% is Alzheimer's disease (AD). AD and delirium, which are known to be aggravated by one another, represent significant societal challenges, especially in light of the absence of effective treatments. The intricate biological mechanisms have led to numerous clinical trial setbacks and likely contribute to the limited efficacy of existing therapeutics. Artificial intelligence (AI) presents a promising avenue for overcoming these hurdles by deploying algorithms to uncover hidden patterns across diverse data types. This review explores the pivotal role of AI in revolutionizing drug discovery for AD and delirium from target identification to the development of small molecule and protein-based therapies. Recent advances in deep learning, particularly in accurate protein structure prediction, are facilitating novel approaches to drug design and expediting the discovery pipeline for biological and small molecule therapeutics. This review concludes with an appraisal of current achievements and limitations, and touches on prospects for the use of AI in advancing drug discovery in AD and delirium, emphasizing its transformative potential in addressing these two and possibly other neurodegenerative conditions.

Indexed as

Alzheimer’s diseaseArtificial intelligenceDeep learningDeliriumDrug discoveryNeurodegenerationTarget identification

Identifiers

PMID41049735
PMCPMC12491689

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.