Evidence map›Paper›PMID 41198459›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2026

Restoration neurite growth by removing the blockage of endosome trafficking in Alzheimer-like mice.

Huimin Zhao, Fangjie Li, Sheng Xu, Yanan Du, Peipei Chen, Jie Wei, Kun Hao, Xiaoquan Liu, Haochen Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Huimin ZhaoSchool of Science, China Pharmaceutical University, Nanjing, 210009, China.
Fangjie LiSchool of Science, China Pharmaceutical University, Nanjing, 210009, China.
Sheng XuCenter of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, 210009, China.
Yanan DuCenter of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, 210009, China.
Peipei ChenCenter of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, 210009, China.
Jie WeiCenter of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, 210009, China.
Kun HaoState Key Laboratory of Natural Medicines, Jiangsu Province Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China. Electronic address: haokun@cpu.edu.cn.
Xiaoquan LiuCenter of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, 210009, China. Electronic address: lxq@cpu.edu.cn.
Haochen LiuCenter of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, 210009, China. Electronic address: haochenliu@cpu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synaptic loss is strongly associated with cognitive decline in Alzheimer's disease (AD). Endosomal trafficking dysfunction, observed in AD brains, impairs neurite growth. Because endosomal trafficking is essential for synaptic development, we selected LMTK1, a negative regulator of Rab11/RE pathway, for this study, given its upregulation in AD models. Clinical genomic data from the ADNI ​(Alzheimer's Disease Neuroimaging Initiative) database were analyzed to evaluate the relationship between LMTK1 and AD. Two AD mouse models, 3xTg and SAMP8, were examined for neurite outgrowth, synaptic density, LMTK1 expression, and recycling endosomes (RE) transport. LMTK1 knockdown was achieved using AAV. The Morris water maze, Golgi staining, immunofluorescence, and electrophysiology experiments were used to assess cognitive function, neurite outgrowth, synaptic density, RE transport, long-term potentiation (LTP), and synaptic transmission. The mechanism of LMTK1 in regulating RE transport was examined through co-immunoprecipitation, proteomics, and point mutation experiments. This study shows that phosphorylated LMTK1 activates TBC1D9B, which deactivates Rab11a and may suppress Rab11a

Indexed as

Alzheimer DiseaseEndosomesNeuritesNeuronal OutgrowthAnimalsDisease Models, AnimalHumansMaleMiceMice, TransgenicAlzheimer's diseaseEndosome traffickingLMTK1Neurite growth

Identifiers

PMID41198459
PMCPMC12976499

What Socratic 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 Socratic graph.