Evidence map›Paper›PMID 41513640›Full record

ReviewCell death & disease2026

Amyloid-β and Tau in Alzheimer's disease: pathogenesis, mechanisms, and interplay.

Altaf A Abdulkhaliq, Bonglee Kim, Yousef M Almoghrabi, Johra Khan, Amir Ajoolabady, Jun Ren, Suhad Bahijri, Jaakko Tuomilehto, Anwar Borai, Domenico Pratico

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

46 citing papers in PubMed.

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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

10 authors.

Altaf A Abdulkhaliq *Department of Biochemistry, Faculty of Medicine, Umm Al-Qura University, Mecca, Saudi Arabia.
Bonglee Kim *Department of Pathology, College of Korean Medicine, Kyung Hee University, Hoegidong Dongdaemun-gu, Seoul, Republic of Korea.
Yousef M Almoghrabi *Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Johra KhanDepartment of Medical Laboratory Sciences, College of Applied Medical Sciences, Majmaah University, Al Majmaah, Saudi Arabia.
Amir AjoolabadyNational Clinical Research Center for Interventional Medicine, Shanghai, China.ORCID http://orcid.org/0000-0002-3667-2605
Jun RenShanghai Institute of Cardiovascular Diseases, Department of Cardiology, Zhongshan Hospital Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-0275-0783
Suhad BahijriDepartment of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Jaakko TuomilehtoDepartment of Public Health, University of Helsinki, Helsinki, Finland.
Anwar BoraiKing Abdullah International Medical Research Center (KAIMRC), King Saud Bin Abdulaziz University for Health Sciences (KSAU-HS), King Abdulaziz Medical City, Ministry of National Guard Health Affairs, Jeddah, Saudi Arabia.
Domenico PraticoDepartment of Neural Sciences, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA. domenico.pratico@temple.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disease and the most prevalent type of dementia characterized by pathological deposition of amyloid-β plaques/deposits and tau tangles within the brain parenchyma. This progressive ailment is featured by irreversible cognitive impairment and memory loss, often misdiagnosed as the consequence of old age in elderlies. Pathologically, synaptic dysfunction occurs at the early stages and then progresses into neurodegeneration with neuronal cell death in later stages. In this review, we aimed to critically discuss and highlight recent advances in the pathological footprints of amyloid-β and tau in AD. Specifically, we focused our attention on the interplay and synergistic effects of amyloid-β and tau in the pathogenesis of AD. We hope that our paper will provide new insights and perspectives on these pathological features of AD and spark new ideas and directions in AD research and treatment.

Indexed as

Alzheimer DiseaseAmyloid beta-Peptidestau ProteinsAnimalsBrainHumansAmyloid beta-Peptidestau Proteins

Identifiers

PMID41513640
PMCPMC12789470

What OpenQuestion holds

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Registered trials

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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.