Evidence map›Paper›PMID 39232848›Full record

ReviewTranslational neurodegeneration2024

Updates in Alzheimer's disease: from basic research to diagnosis and therapies.

Enjie Liu, Yao Zhang, Jian-Zhi Wang

Abstract readReview
In one paragraph

Review in Translational neurodegeneration, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 2 pooled it
–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

111 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  19. Multicenter validation of plasma p-tau217/ amyloid beta 1-42 ratio in symptomatic Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  20. Lecanemab treatment improves B cell subpopulation immune homeostasis in patients with Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article

51 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

3 authors.

Enjie LiuDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Yao ZhangDepartment of Endocrine, Liyuan Hospital, Key Laboratory of Ministry of Education for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430077, China.
Jian-Zhi WangDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. wangjz@mail.hust.edu.cn.ORCID 0000-0002-0181-4415

Funding

National Natural Science Foundation of China 1949205National Natural Science Foundation of China 31730035National Natural Science Foundation of China 81721005National Natural Science Foundation of China 82001134Natural Science Foundation of Henan Province 242300421081the Guangdong Provincial Key S&T Program 018B030336001
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disorder, characterized pathologically by extracellular deposition of β-amyloid (Aβ) into senile plaques and intracellular accumulation of hyperphosphorylated tau (pTau) as neurofibrillary tangles. Clinically, AD patients show memory deterioration with varying cognitive dysfunctions. The exact molecular mechanisms underlying AD are still not fully understood, and there are no efficient drugs to stop or reverse the disease progression. In this review, we first provide an update on how the risk factors, including APOE variants, infections and inflammation, contribute to AD; how Aβ and tau become abnormally accumulated and how this accumulation plays a role in AD neurodegeneration. Then we summarize the commonly used experimental models, diagnostic and prediction strategies, and advances in periphery biomarkers from high-risk populations for AD. Finally, we introduce current status of development of disease-modifying drugs, including the newly officially approved Aβ vaccines, as well as novel and promising strategies to target the abnormal pTau. Together, this paper was aimed to update AD research progress from fundamental mechanisms to the clinical diagnosis and therapies.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBiomarkersHumanstau ProteinsAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer’s diseaseDiagnosisDrug developmentNeurodegenerationTauβ-Amyloid

Identifiers

PMID39232848
PMCPMC11373277

What Socratic holds

Textmetadata
LicenceCC BY
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.