Evidence map›Paper›PMID 35596894›Full record

ArticleNeuroscience bulletin2022

cPKCγ Deficiency Exacerbates Autophagy Impairment and Hyperphosphorylated Tau Buildup through the AMPK/mTOR Pathway in Mice with Type 1 Diabetes Mellitus.

Jiayin Zheng, Yue Wang, Yue Liu, Song Han, Ying Zhang, Yanlin Luo, Yi Yan, Junfa Li, Li Zhao

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. The connection between autophagy and Alzheimer's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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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

9 authors at 1 institution in 1 country.

Jiayin Zheng *Department of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China.
Yue Wang *The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Capital Medical University, Beijing, 100088, China.
Yue LiuDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China.
Song HanDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China.
Ying ZhangDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China.
Yanlin LuoDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China.
Yi YanDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China.
Junfa LiDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China. junfali@ccmu.edu.cn.ORCID https://orcid.org/0000-0002-1930-9724
Li ZhaoDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China. zhaoli@ccmu.edu.cn.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes mellitus (T1DM)-induced cognitive dysfunction is common, but its underlying mechanisms are still poorly understood. In this study, we found that knockout of conventional protein kinase C (cPKC)γ significantly increased the phosphorylation of Tau at Ser214 and neurofibrillary tangles, but did not affect the activities of GSK-3β and PP2A in the hippocampal neurons of T1DM mice. cPKCγ deficiency significantly decreased the level of autophagy in the hippocampal neurons of T1DM mice. Activation of autophagy greatly alleviated the cognitive impairment induced by cPKCγ deficiency in T1DM mice. Moreover, cPKCγ deficiency reduced the AMPK phosphorylation levels and increased the phosphorylation levels of mTOR in vivo and in vitro. The high glucose-induced Tau phosphorylation at Ser214 was further increased by the autophagy inhibitor and was significantly decreased by an mTOR inhibitor. In conclusion, these results indicated that cPKCγ promotes autophagy through the AMPK/mTOR signaling pathway, thus reducing the level of phosphorylated Tau at Ser214 and neurofibrillary tangles.

Indexed as

AMP-Activated Protein KinasesDiabetes Mellitus, Type 1AnimalsAutophagyGlucoseGlycogen Synthase Kinase 3 betaMicePhosphorylationProtein Kinase Ctau ProteinsTOR Serine-Threonine KinasesAMP-Activated Protein KinasesGlucoseGlycogen Synthase Kinase 3 betaProtein Kinase Ctau ProteinsTOR Serine-Threonine KinasesAMPK/mTOR signaling pathwayAutophagyConventional protein kinase C (cPKC)γPhosphorylated TauTau

Identifiers

PMID35596894
PMCPMC9554100
OpenAlexW4281254985

What Socratic 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 Socratic graph.