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Amyloid beta and diabetic pathology cooperatively stimulate cytokine expression in an Alzheimer’s mouse model

Overview of attention for article published in Journal of Neuroinflammation, January 2020
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  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (81st percentile)

Mentioned by

1 news outlet
1 tweeter


17 Dimensions

Readers on

57 Mendeley
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Amyloid beta and diabetic pathology cooperatively stimulate cytokine expression in an Alzheimer’s mouse model
Published in
Journal of Neuroinflammation, January 2020
DOI 10.1186/s12974-020-1707-x
Pubmed ID

Sitara B. Sankar, Carmen Infante-Garcia, Laura D. Weinstock, Juan Jose Ramos-Rodriguez, Carmen Hierro-Bujalance, Cecilia Fernandez-Ponce, Levi B. Wood, Monica Garcia-Alloza


Diabetes is a risk factor for developing Alzheimer's disease (AD); however, the mechanism by which diabetes can promote AD pathology remains unknown. Diabetes results in diverse molecular changes in the brain, including dysregulation of glucose metabolism and loss of cerebrovascular homeostasis. Although these changes have been associated with increased Aβ pathology and increased expression of glial activation markers in APPswe/PS1dE9 (APP/PS1) mice, there has been limited characterization, to date, of the neuroinflammatory changes associated with diabetic conditions. To more fully elucidate neuroinflammatory changes associated with diabetes that may drive AD pathology, we combined the APP/PS1 mouse model with either high-fat diet (HFD, a model of pre-diabetes), the genetic db/db model of type 2 diabetes, or the streptozotocin (STZ) model of type 1 diabetes. We then used a multiplexed immunoassay to quantify cortical changes in cytokine proteins. Our analysis revealed that pathology associated with either db/db, HFD, or STZ models yielded upregulation of a broad profile of cytokines, including chemokines (e.g., MIP-1α, MIP-1β, and MCP-1) and pro-inflammatory cytokines, including IL-1α, IFN-γ, and IL-3. Moreover, multivariate partial least squares regression analysis showed that combined diabetic-APP/PS1 models yielded cooperatively enhanced expression of the cytokine profile associated with each diabetic model alone. Finally, in APP/PS1xdb/db mice, we found that circulating levels of Aβ1-40, Aβ1-42, glucose, and insulin all correlated with cytokine expression in the brain, suggesting a strong relationship between peripheral changes and brain pathology. Altogether, our multiplexed analysis of cytokines shows that Alzheimer's and diabetic pathologies cooperate to enhance profiles of cytokines reported to be involved in both diseases. Moreover, since many of the identified cytokines promote neuronal injury, Aβ and tau pathology, and breakdown of the blood-brain barrier, our data suggest that neuroinflammation may mediate the effects of diabetes on AD pathogenesis. Therefore, strategies targeting neuroinflammatory signaling, as well as metabolic control, may provide a promising strategy for intervening in the development of diabetes-associated AD.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 57 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 57 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 12 21%
Student > Ph. D. Student 8 14%
Student > Master 6 11%
Student > Bachelor 3 5%
Student > Doctoral Student 3 5%
Other 11 19%
Unknown 14 25%
Readers by discipline Count As %
Medicine and Dentistry 9 16%
Biochemistry, Genetics and Molecular Biology 8 14%
Neuroscience 4 7%
Pharmacology, Toxicology and Pharmaceutical Science 4 7%
Unspecified 3 5%
Other 13 23%
Unknown 16 28%

Attention Score in Context

This research output has an Altmetric Attention Score of 10. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 03 February 2020.
All research outputs
of 16,750,089 outputs
Outputs from Journal of Neuroinflammation
of 2,092 outputs
Outputs of similar age
of 328,900 outputs
Outputs of similar age from Journal of Neuroinflammation
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Altmetric has tracked 16,750,089 research outputs across all sources so far. Compared to these this one has done well and is in the 86th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 2,092 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.7. This one has gotten more attention than average, scoring higher than 74% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 328,900 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 81% of its contemporaries.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them