Evidence map›Paper›PMID 34471085›Full record

ReviewMedical science monitor : international medical journal of experimental and clinical research2021

The Role of Amyloid-Beta and Tau in the Early Pathogenesis of Alzheimer's Disease.

Xiaomin Yin, Yanyan Qiu, Chenhao Zhao, Zheng Zhou, Junze Bao, Wei Qian

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Medical science monitor : international medical journal of experimental and clinical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Neuroinflammation and Tauopathies.Molecular biology reports · 2026
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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

6 authors at 1 institution in 1 country.

Xiaomin YinDepartment of Biochemistry and Molecular Biology, Medical School, Nantong University, Nantong, Jiangsu, China (mainland).
Yanyan QiuDepartment of Biochemistry and Molecular Biology, Medical School, Nantong University, Nantong, Jiangsu, China (mainland).
Chenhao ZhaoDepartment of Biochemistry and Molecular Biology, Medical School, Nantong University, Nantong, Jiangsu, China (mainland).
Zheng ZhouDepartment of Biochemistry and Molecular Biology, Medical School, Nantong University, Nantong, Jiangsu, China (mainland).
Junze BaoDepartment of Biochemistry and Molecular Biology, Medical School, Nantong University, Nantong, Jiangsu, China (mainland).
Wei QianDepartment of Biochemistry and Molecular Biology, Medical School, Nantong University, Nantong, Jiangsu, China (mainland).
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The abnormal accumulation of amyloid-b (Ab) and neurofibrillary tangles (NFTs) containing phosphorylated tau proteins are the main histopathological feature of Alzheimer's disease (AD). Synaptic damage and loss are earlier events than amyloid plaques and NFTs in AD progress and best correlate with cognitive deficits in AD patients. Soluble oligomeric Aß initiates the progression of AD and tau mediates the subsequent synaptic impairments at an early stage of AD. In this review we discuss how Ab or/and tau causes synaptic dysfunction. Ab oligomers gather at synapses and give rise to synaptic death in a variety of ways such as regulating receptors and receptor tyrosine kinases, unbalancing calcium homeostasis, and activating caspases and calcineurin. A large amount of hyperphosphorylated tau exists in the synapse of the AD brain. Aß-triggered synaptic deficits are dependent on tau. Soluble, hyperphosphorylated tau is much more correlated to cognitive decline in AD patients. Tau-targeted therapies have received more attention because the treatments targeting Aß failed in AD. Here, we also review the therapy strategies used to intervene in the very early stages of AD. Soluble hyperphosphorylated tau forms a complex with cell surface receptors, scaffold proteins, or intracellular signaling molecules to damage synaptic function. Therefore, therapeutic strategies targeting synaptic tau at the early stage of AD may ameliorating pathology in AD. This review aims to provide an update on the role of oligomeric Ab and soluble hyperphosphorylated tau in the early pathogenesis of Alzheimer's disease and to develop a new treatment strategy based on this.

Indexed as

SynapsesAlzheimer DiseaseAmyloid beta-PeptidesAnimalsHumanstau ProteinsAmyloid beta-Peptidestau Proteins

Identifiers

PMID34471085
PMCPMC8422899
OpenAlexW3170071980

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.