Evidence map›Paper›PMID 26298663›Full record

ReviewMolecular neurobiology2016

Streptozotocin Intracerebroventricular-Induced Neurotoxicity and Brain Insulin Resistance: a Therapeutic Intervention for Treatment of Sporadic Alzheimer's Disease (sAD)-Like Pathology.

Pradip K Kamat, Anuradha Kalani, Shivika Rai, Santosh Kumar Tota, Ashok Kumar, Abdullah S Ahmad

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

75 citing papers in PubMed, 144 citations in OpenAlex.

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15 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

6 authors at 3 institutions in 2 countries.

Pradip K KamatDepartment of Anesthesiology, Center for Translational Research in Neurodegenerative Disease (CTRND), College of Medicin, University of Florida, Gainesville, FL, 32610, USA. pradeepkamat2004@gmail.com.
Anuradha KalaniDivision of Physiology and Biophysics, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
Shivika RaiDivision of Pharmacology, CSIR-Central drug Research Institute (CDRI), Lucknow, 226031, India.
Santosh Kumar TotaDivision of Pharmacology, CSIR-Central drug Research Institute (CDRI), Lucknow, 226031, India.
Ashok KumarMcKnight Brain Institute, University of Florida, Gainesville, FL, 32610, USA.
Abdullah S AhmadDepartment of Anesthesiology, Center for Translational Research in Neurodegenerative Disease (CTRND), College of Medicin, University of Florida, Gainesville, FL, 32610, USA.
University of Florida · USCentral Drug Research Institute · INUniversity of Louisville · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder that is remarkably characterized by pathological hallmarks which include amyloid plaques, neurofibrillary tangles, neuronal loss, and progressive cognitive loss. Several well-known genetic mutations which are being used for the development of a transgenic model of AD lead to an early onset familial AD (fAD)-like condition. However, these settings are only reasons for a small percentage of the total AD cases. The large majorities of AD cases are considered as a sporadic in origin and are less influenced by a single mutation of a gene. The etiology of sporadic Alzheimer's disease (sAD) remains unclear, but numerous risk factors have been identified that increase the chance of developing AD. Among these risk factors are insulin desensitization/resistance state, oxidative stress, neuroinflammation, synapse dysfunction, tau hyperphosphorylation, and deposition of Aβ in the brain. Subsequently, these risk factors lead to development of sAD. However, the underlying molecular mechanism is not so clear. Streptozotocin (STZ) produces similar characteristic pathology of sAD such as altered glucose metabolism, insulin signaling, synaptic dysfunction, protein kinases such as protein kinase B/C, glycogen synthase-3β (GSK-3β) activation, tau hyperphosphorylation, Aβ deposition, and neuronal apoptosis. Further, STZ also leads to inhibition of Akt/PKB, insulin receptor (IR) signaling molecule, and insulin resistance in brain. These alterations mediated by STZ can be used to explore the underlying molecular and pathophysiological mechanism of AD (especially sAD) and their therapeutic intervention for drug development against AD pathology.

Indexed as

Disease Models, AnimalAlzheimer DiseaseAnimalsBrainHumansInjections, IntraventricularInsulin ResistanceOxidative StressStreptozocinTreatment OutcomeStreptozocinAlzheimer’s diseaseInsulinKinaseNeuroinflammationStreptozotocin

Identifiers

PMID26298663
OpenAlexW1198964477

What OpenQuestion holds

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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.