Evidence map›Paper›PMID 25934036›Full record

ReviewNeuroscience2015

Models and mechanisms for hippocampal dysfunction in obesity and diabetes.

A M Stranahan

Abstract readReview
In one paragraph

Review in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
–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

53 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  6. Muscle-Derived miR-200a-3p Through Light-Intensity Exercise May Contribute to Improve Memory Dysfunction in Type 2 Diabetic Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 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

1 author.

A M StranahanDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Georgia Regents University, 1120 15th Street, Room CA3064, Augusta, GA 30912, United States. Electronic address: astranahan@gru.edu.

Funding

Hippocampal Dysfunction Prolongs Stress Responses in Leptin Receptor Mutant MiceR03DK101817 · NIDDK · AUGUSTA UNIVERSITY · PI STRANAHAN, ALEXIS M. · 2014 to 2016
$569k
Adipose inflammation mediates obesity-induced deficits in hippocampal plasticityK01DK100616 · NIDDK · AUGUSTA UNIVERSITY · PI STRANAHAN, ALEXIS M. · 2013 to 2015
$369k
NIDDK NIH HHS K01 DK100616NIDDK NIH HHS K01DK100616NIDDK NIH HHS R03 DK101817NIDDK NIH HHS R03DK101817
6 · The paper itself

Abstract

Clinical studies suggest that obesity and Type 2 (insulin-resistant) diabetes impair the structural integrity of medial temporal lobe regions involved in memory and confer greater vulnerability to neurological insults. While eliminating obesity and its endocrine comorbidities would be the most straightforward way to minimize cognitive risk, structural barriers to physical activity and the widespread availability of calorically dense, highly palatable foods will likely necessitate additional strategies to maintain brain health over the lifespan. Research in rodents has identified numerous correlates of hippocampal functional impairment in obesity and diabetes, with several studies demonstrating causality in subsequent mechanistic studies. This review highlights recent work on pathways and cell-cell interactions underlying the synaptic consequences of obesity, diabetes, or in models with both pathological conditions. Although the mechanisms vary across different animal models, immune activation has emerged as a shared feature of obesity and diabetes, with synergistic exacerbation of neuroinflammation in model systems with both conditions. This review discusses these findings with reference to the benefits of incorporating existing models from the fields of obesity and metabolic disease. Many transgenic lines with basal metabolic alterations or differential susceptibility to diet-induced obesity have yet to be characterized with respect to their cognitive and synaptic phenotype. Adopting these models, and building on the extensive knowledge base used to generate them, is a promising avenue for understanding interactions between peripheral disease states and neurodegenerative disorders.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2HippocampusHumansNeuroimmunomodulationNeuronal PlasticityObesitydiabeteshippocampusinsulin resistancelong-term potentiationobesitysynapse

Identifiers

PMID25934036
PMCPMC4624614

What OpenQuestion holds

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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.