Evidence map›Paper›PMID 39751702›Full record

ReviewNeuromolecular medicine2024

The Interplay Between Accumulation of Amyloid-Beta and Tau Proteins, PANoptosis, and Inflammation in Alzheimer's Disease.

Xianbo Zhuang, Jie Lin, Yamin Song, Ru Ban, Xin Zhao, Zhangyong Xia, Zheng Wang, Guifeng Zhang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neuromolecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. The evolving landscape of amyloid-targeting therapies in Alzheimer's disease: progress and challenges.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  5. Genomic and proteomic conversion of brain ischemia to Alzheimer's disease.Frontiers in cell and developmental biology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. 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

8 authors.

Xianbo Zhuang *Department of Neurology, Liaocheng People's Hospital and Liaocheng Hospital Affiliated to Shandong First Medical University, Liaocheng, 252000, China.
Jie Lin *School of Basic Medicine Sciences, Shandong University, Jinan, China.
Yamin SongDepartment of Neurology, Liaocheng People's Hospital and Liaocheng Hospital Affiliated to Shandong First Medical University, Liaocheng, 252000, China.
Ru BanDepartment of Neurology, Liaocheng People's Hospital and Liaocheng Hospital Affiliated to Shandong First Medical University, Liaocheng, 252000, China.
Xin ZhaoDepartment of Neurology, Liaocheng People's Hospital and Liaocheng Hospital Affiliated to Shandong First Medical University, Liaocheng, 252000, China.
Zhangyong XiaDepartment of Neurology, Liaocheng People's Hospital and Liaocheng Hospital Affiliated to Shandong First Medical University, Liaocheng, 252000, China. xiazhangyong2013@163.com.
Zheng WangDepartment of Neurosurgery, Liaocheng Traditional Chinese Medicine Hospital, Liaocheng, 252000, China. zhengyimingdao@gmail.com.
Guifeng ZhangDepartment of Neurology, Liaocheng People's Hospital and Liaocheng Hospital Affiliated to Shandong First Medical University, Liaocheng, 252000, China. GFZhangNo.1@gmail.com.

Funding

Liaocheng Key Research and Development Plan 2022YDSF26Shandong Society of Geriatrics Scientific and Technological Research Project LKJGG2021W067
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a common progressive neurodegenerative disorder, and the vast majority of cases occur in elderly patients. Recently, the accumulation of Aβ and tau proteins has drawn considerable attention in AD research. This review explores the multifaceted interactions between these proteins and their contribution to the pathological landscape of AD, encompassing synaptic dysfunction, neuroinflammation, and PANoptosis. PANoptosis is a collective term for programmed cell death (PCD) modalities that encompass elements of apoptosis, pyroptosis, and necroptosis. The accumulation of Aβ peptides and tau proteins, along with the immune response in brain cells, may trigger PANoptosis, thus advancing the progression of the disease. Recent advancements in molecular imaging and genetics have provided deeper insights into the interactions between Aβ peptides, tau proteins, and the immune response. The review also discusses the role of mitochondrial dysregulation in AD. The exploration of the interplay between neurodegeneration, immune responses, and cell death offers promising avenues for the development of innovative treatments.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesApoptosisNecroptosisNeuroinflammatory DiseasesPyroptosistau ProteinsAnimalsBrainHumansMitochondriaAmyloid beta-PeptidesMAPT protein, humantau ProteinsAlzheimer’s diseaseAmyloid-betaInflammationPANoptosisTau proteinTherapeutic strategy

Identifiers

What Socratic holds

Textmetadata
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 Socratic graph.