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Cited by 87Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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

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Abdulkhaliq, Altaf A., Kim, Bonglee, Almoghrabi, Yousef M., Khan, Johra, Ajoolabady, Amir, Ren, Jun, Bahijri, Suhad, Tuomilehto, Jaakko +2 more·2026·Cell Death & Disease
DOI 10.1038/s41419-025-08186-8PMC PMC12789470
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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.

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  • Microglia are central regulators of Alzheimer's disease pathogenesis, and their roles cannot be reduced to a simple protective-versus-harmful dichotomy.

    “Microglia are central regulators of Alzheimer’s disease pathogenesis, but their roles cannot be reduced to a simple protective-versus-harmful dichotomy.”

    From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [1]

    The section “Microglia and GSK3β-mediated phosphorylation of tau” (page unavailable) describes microglia as governing CNS homeostasis and identifies a microglia-mediated mechanism that protects against tau pathology in Alzheimer’s disease. It does not establish that microglia are central regulators of Alzheimer’s pathogenesis or discuss why their roles cannot be reduced to a protective-versus-harmful dichotomy. (LLM, conf=0.82)

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Authors
Abdulkhaliq, A. A., Kim, B., Almoghrabi, Y. M., Khan, J., Ajoolabady, A., Ren, J., Bahijri, S., Tuomilehto, J., Borai, A., & Pratico, D.
Affiliations
  • Umm al-Qura University (SA)
  • Kyung Hee University (KR)
  • King Abdulaziz University (SA)
  • Majmaah University (SA)
  • Fudan University (CN)
  • University of Helsinki (FI)
  • King Saud bin Abdulaziz University for Health Sciences (SA)
ORCID
Venue
Cell Death & Disease
Publisher
Springer Science and Business Media LLC
Published
2026-01-09
Volume
17
Issue
1
Pages
21-21
ISSN
2041-4889 (ISSN-L)
DOI
10.1038/s41419-025-08186-8
PMC
PMC12789470
OpenAlex
W7119988617
Cited by
87
References
119
Citations by year
2026: 87
FWCI
91.00
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Death and Disease (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • PubMed Central (publishedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Työväentutkimus Vuosikirja (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, amyloid-beta, tau protein, amyloid plaques, tau tangles, synaptic dysfunction, neurodegeneration, neuronal cell death, pathogenesis, cognitive impairment
MeSH terms
Alzheimer Disease, Animals, Brain, Humans, Amyloid beta-Peptides, tau Proteins

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