Evidence map›Paper›PMID 29626319›Full record

ReviewNeurotoxicity research2018

Clearance of Amyloid Beta and Tau in Alzheimer's Disease: from Mechanisms to Therapy.

Shu-Hui Xin, Lin Tan, Xipeng Cao, Jin-Tai Yu, Lan Tan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 2 pooled it
8.6field-weighted citation impact, top 1% of its field
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

108 citing papers in PubMed, 2 syntheses or guidelines pooled it, 205 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Choroid plexus remodeling linked to impaired CSF-mediated clearance and Alzheimer's disease progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Opposing patterns of blood-brain barrier permeability and Alzheimer's disease biomarkers across APOE genotype.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  10. The gut as a central hub for multi-organ crosstalk in aging.Cellular and molecular life sciences : CMLS · 2026
    Review
  11. Article
  12. Choroidal-ventricular system abnormalities are linked to amyloid-β aggregation in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. The connection between autophagy and Alzheimer's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  18. Review
  19. Article
  20. Review

48 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Shu-Hui XinDepartment of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, No.5 Donghai Middle Road, Qingdao, 266071, Shandong, China.
Lin TanDepartment of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, No.5 Donghai Middle Road, Qingdao, 266071, Shandong, China.
Xipeng CaoClinical Research Center, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.
Jin-Tai YuDepartment of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, No.5 Donghai Middle Road, Qingdao, 266071, Shandong, China. yu-jintai@163.com.
Lan TanDepartment of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, No.5 Donghai Middle Road, Qingdao, 266071, Shandong, China. dr.tanlan@163.com.
Qingdao Municipal Hospital · CNQingdao University · CN

Funding

National key projects for research and development of MOST 2016YFC1305800
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease. Pathological proteins of AD mainly contain amyloid-beta (Aβ) and tau. Their deposition will lead to neuron damage by a series of pathways, and then induce memory and cognitive impairment. Thus, it is pivotal to understand the clearance pathways of Aβ and tau in order to delay or even halt AD. Aβ clearance mechanisms include ubiquitin-proteasome system, autophagy-lysosome, proteases, microglial phagocytosis, and transport from the brain to the blood via the blood-brain barrier (BBB), arachnoid villi and blood-CSF barrier, which can be named blood circulatory clearance. Recently, lymphatic clearance has been demonstrated to play a key role in transport of Aβ into cervical lymph nodes. The discovery of meningeal lymphatic vessels is another direct evidence for lymphatic clearance in the brain. Furthermore, periphery clearance also contributes to Aβ clearance. Tau clearance is almost the same as Aβ clearance. In this review, we will mainly introduce the clearance mechanisms of Aβ and tau proteins, and summarize corresponding targeted drug therapies for AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsHumanstau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer’s diseaseAmyloid-betaBlood circulatory clearanceLymphatic clearancePeripheral clearanceTau

Identifiers

PMID29626319
OpenAlexW2795597697

What OpenQuestion 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 OpenQuestion graph.