Evidence map›Paper›PMID 27457264›Full record

ArticleAging cell2016

Intranasal insulin alleviates cognitive deficits and amyloid pathology in young adult APPswe/PS1dE9 mice.

Yan-Fang Mao, Zhangyu Guo, Tingting Zheng, Yasi Jiang, Yaping Yan, Xinzhen Yin, Yanxing Chen, Baorong Zhang

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 2 pooled it
7.2field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 108 citations in OpenAlex.

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  5. Insulin resistance: fueling oxidative stress and neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2025
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8 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

8 authors at 1 institution in 1 country.

Yan-Fang MaoDepartment of Neurology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Zhangyu GuoDepartment of Neurology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Tingting ZhengDepartment of Neurology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Yasi JiangDepartment of Neurology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Yaping YanDepartment of Neurology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Xinzhen YinDepartment of Neurology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Yanxing ChenDepartment of Neurology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Baorong ZhangDepartment of Neurology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Second Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain insulin signaling deficits contribute to multiple pathological features of Alzheimer's disease (AD). Although intranasal insulin has shown efficacy in patients with AD, the underlying mechanisms remain largely unillustrated. Here, we demonstrate that intranasal insulin improves cognitive deficits, ameliorates defective brain insulin signaling, and strongly reduces β-amyloid (Aβ) production and plaque formation after 6 weeks of treatment in 4.5-month-old APPswe/PS1dE9 (APP/PS1) mice. Furthermore, c-Jun N-terminal kinase activation, which plays a pivotal role in insulin resistance and AD pathologies, is significantly inhibited. The alleviation of amyloid pathology by intranasal insulin results mainly from enhanced nonamyloidogenic processing and compromised amyloidogenic processing of amyloid precursor protein (APP), and from a reduction in apolipoprotein E protein which is involved in Aβ metabolism. In addition, intranasal insulin effectively promotes hippocampal neurogenesis in APP/PS1 mice. This study, exploring the mechanisms underlying the beneficial effects of intranasal insulin on Aβ pathologies in vivo for the first time, highlights important preclinical evidence that intranasal insulin is potentially an effective therapeutic method for the prevention and treatment of AD.

Indexed as

Administration, IntranasalAgingAmyloidAmyloid beta-Protein PrecursorAnimalsAnxietyCognition DisordersEnzyme ActivationHumansInsulinJNK Mitogen-Activated Protein KinasesMemoryMice, TransgenicNeurogenesisPlaque, AmyloidPresenilin-1AmyloidAmyloid beta-Protein PrecursorInsulinJNK Mitogen-Activated Protein KinasesPresenilin-1Alzheimer's diseaseamyloid pathologyAPP processingAPP/PS1insulin signaling

Identifiers

PMID27457264
PMCPMC5013027
OpenAlexW2501462863

What OpenQuestion 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 OpenQuestion graph.