Evidence map›Paper›PMID 39971888›Full record

ArticleNeuroscience bulletin2025

Fibrinogen-tau Aggregates Exacerbate Tau Pathology and Memory Deficits in Alzheimer's Disease Model Mice.

Tingting Wen, Lanxia Meng, Han Liu, Qian Zhang, Lijun Dai, Liqin Huang, Liang Dan, Kedong Zhu, Jiaying Luo, Zhaohui Zhang

Abstract read
In one paragraph

Article in Neuroscience bulletin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. CSF fibrinogen predicts longitudinal Tau accumulation in cognitively unimpaired older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  3. Unveiling the procoagulant state in Alzheimer's disease: A novel PET imaging strategy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  4. Article
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

10 authors.

Tingting Wen *Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Lanxia Meng *Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Han Liu *Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Qian ZhangDepartment of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Lijun DaiDepartment of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Liqin HuangDepartment of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Liang DanDepartment of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Kedong ZhuDepartment of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Jiaying LuoDepartment of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Zhaohui ZhangDepartment of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, China. zhzhqing1990@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular damage plays a significant role in the onset and progression of Alzheimer's disease (AD). However, the precise molecular mechanisms underlying the induction of neuronal injury by vascular damage remain unclear. The present study aimed to examine the impact of fibrinogen (Fg) on tau pathology. The results showed that Fg deposits in the brains of tau P301S transgenic mice interact with tau, enhancing the cytotoxicity of pathological tau aggregates and promoting tau phosphorylation and aggregation. Notably, Fg-modified tau fibrils caused enhanced neuronal apoptosis and synaptic damage compared to unmodified fibrils. Furthermore, intrahippocampal injection of Fg-modified tau fibrils worsened the tau pathology, neuroinflammation, synaptic damage, neuronal apoptosis, and cognitive dysfunction in tau P301S mice compared to controls. The present study provides compelling evidence linking Fg and tau, thereby connecting cerebrovascular damage to tau pathology in AD. Consequently, inhibiting Fg-mediated tau pathology could potentially impede the progression of AD.

Indexed as

Alzheimer DiseaseFibrinogenMemory Disorderstau ProteinsAnimalsApoptosisBrainDisease Models, AnimalHippocampusMaleMiceMice, Inbred C57BLMice, TransgenicPhosphorylationProtein Aggregation, PathologicalFibrinogenMapt protein, mousetau ProteinsAlzheimer’s diseaseCross-seedingFibrinogenTauopathy

Identifiers

PMID39971888
PMCPMC12229364

What OpenQuestion holds

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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.