Evidence map›Paper›PMID 27730514›Full record

ArticleMolecular neurobiology2017

Intranasal Insulin Administration Ameliorates Streptozotocin (ICV)-Induced Insulin Receptor Dysfunction, Neuroinflammation, Amyloidogenesis, and Memory Impairment in Rats.

N Rajasekar, Chandishwar Nath, Kashif Hanif, Rakesh Shukla

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Review
  6. Time- and Region-Specific Effects of Intranasal Insulin on Oxidative Stress Parameters in the Rat Brain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  18. Nose-to-brain drug delivery: from bench to bedside.Translational neurodegeneration · 2025
    Review
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  20. Article

2 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

4 authors at 2 institutions in 1 country.

N RajasekarDivisions of Pharmacology and Toxicology, CSIR-Central Drug Research Institute, Lucknow, 226031, India.
Chandishwar NathDivisions of Pharmacology and Toxicology, CSIR-Central Drug Research Institute, Lucknow, 226031, India.
Kashif HanifDivisions of Pharmacology and Toxicology, CSIR-Central Drug Research Institute, Lucknow, 226031, India.
Rakesh ShuklaDivisions of Pharmacology and Toxicology, CSIR-Central Drug Research Institute, Lucknow, 226031, India. rakeshshuklacdri@gmail.com.
Central Drug Research Institute · INAcademy of Scientific and Innovative Research · IN

Funding

Department of Biotechnology, New Delhi BT/PR4012/MED/ 30/672/201 Dated 28/03/2012
6 · The paper itself

Abstract

Alzheimer's disease (AD) is associated with reduced insulin level and impairment of insulin receptor (IR) signaling in the brain, which correlates to amyloid pathology, neuroinflammation, and synaptic neurotoxicity. Clinical studies show that intranasal insulin improves memory in AD patients without peripheral hypoglycemia. However, neuroprotective molecular mechanism of the beneficial effect of intranasal insulin in AD pathology is unexplored. Therefore, we investigated the role of intranasal insulin on intracerebroventricular (ICV) streptozotocin (STZ)-induced memory impairment in rats as evaluated in the Morris water maze test. STZ (ICV) treated rats had shown memory impairment along with a significant decrease in IR signaling molecules (IR, pIRS-1, pAkt, and pGSK-3α/β expression) and IDE expression in both hippocampus and cerebral cortex. Intranasal insulin delivery prevented these changes. Moreover, intranasal insulin was found to inhibit significantly glial cell activation (GFAP and Iba-1 expression), neuroinflammation (COX-2 expression, NFκB translocation, TNF-α, and IL-10 level) and amyloidogenic protein expression (BACE-1 and Aβ

Indexed as

Administration, IntranasalAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesAstrocytesCerebral CortexCytokinesDown-RegulationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHippocampusHypoglycemic AgentsInflammationInsulinInsulin Receptor Substrate ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)Amyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBace1 protein, ratCytokinesGlycogen Synthase Kinase 3glycogen synthase kinase 3 alphaGlycogen Synthase Kinase 3 betaHypoglycemic AgentsInsulinInsulin Receptor Substrate ProteinsIrs1 protein, ratNF-kappa BPeptide FragmentsProto-Oncogene Proteins c-aktReceptor, InsulinStreptozocinAmyloidogenic protein expressionGlial activationInsulin receptor dysfunctionIntranasal insulinpost synaptic neurotoxicity

Identifiers

PMID27730514
OpenAlexW2531062701

What OpenQuestion 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 OpenQuestion graph.