Evidence map›Paper›PMID 41652508›Full record

ArticleJournal of neuroinflammation2026

Sex specific effects of a high fat diet on metabolism, cognition, and pathology in the Tg-SwDI mouse model of Alzheimer's disease.

Shelby Sabourin, Christina A Thrasher, Rachel M Smith, Kasey Belanger-Mayer, Bryce Thibodeau, Charly Abi-Ghanem, Jennifer J Lafrican, Celine Camon, Richard D Kelly, Riane Richard and 9 more

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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

  1. Pooled it
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors.

Shelby SabourinDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Christina A ThrasherDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Rachel M SmithDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Kasey Belanger-MayerDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Bryce ThibodeauDepartment of Regenerative and Cancer Cell Biology, Albany Medical College, Albany, NY, 12208, USA.
Charly Abi-GhanemDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Jennifer J LafricanDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Celine CamonDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Richard D KellyDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Riane RichardDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Abigail E SalineroDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Molly R BatchelderDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Emily A GroomDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA.
Olivia J GannonDepartment of Immunology and Microbial Disease, Albany Medical College, Albany, NY, 12208, USA.
Rachel GrazdaDepartment of Immunology and Microbial Disease, Albany Medical College, Albany, NY, 12208, USA.
Katherine C MacNamaraDepartment of Immunology and Microbial Disease, Albany Medical College, Albany, NY, 12208, USA.
Sally TempleNeural Stem Cell Institute, Albany, NY, 12208, USA.
Kevin PumigliaDepartment of Regenerative and Cancer Cell Biology, Albany Medical College, Albany, NY, 12208, USA. pumiglk@amc.edu.
Kristen L ZuloagaDepartment of Neuroscience and Experimental Therapeutics , Albany Medical College, 12208, Albany, NY, USA. zuloagk@amc.edu.

Funding

Investigating the Functional Impact of AD Risk Genes on Neuro-Vascular InteractionsU01AG072464 · NIA · REGENERATIVE RESEARCH FOUNDATION · PI HARARI, OSCAR, KAMPMANN, MARTIN · 2021 to 2025
$8.7M
Metabolic and Hormonal Mechanisms of VCIDR01NS110749 · NINDS · ALBANY MEDICAL COLLEGE · PI Kristen Leanne Zuloaga · 2019 to 2026
$4.3M
Alzheimer's Association AARG-21-849204American Heart Association 908879BrightFocus Foundation A2022001FNIA NIH HHS U01 AG072464NIH HHS AG072464NINDS NIH HHS R01 NS110749
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is the leading cause of dementia in the US, with over 80% of affected individuals experiencing comorbid metabolic disease. Along with age and sex, metabolic syndrome and prediabetes are known risk factors for developing dementia and AD, highlighting the complex nature of the disease. How these risk factors affect cerebral amyloid angiopathy (CAA) is less well studied. As such, we examined the effect of diet-induced metabolic syndrome and sex on cognition, neuroinflammation, and pathology in the Tg-SwDI mouse model of AD and CAA.

methodsMale and female Tg-SwDI and WT mice were fed a low fat (LFD; 10% fat) or high fat (HFD; 60% fat) diet from 3 to 10 months of age. Metabolic, cognitive, and neuropathology outcomes were assessed.

resultsAll HFD-fed mice gained weight and exhibited impaired glucose tolerance. Metabolic disturbances were most severe in AD females receiving HFD. In both males and females, HFD-fed AD mice showed increased anxiety-like behavior, decreased locomotor activity, and impaired recognition memory in the open field and novel object recognition tests, respectively. HFD-fed AD females specifically exhibited spatial memory deficits in the Barnes maze. Hippocampal microgliosis, activated microglia, and astrogliosis were more severe in AD mice, HFD decreased hippocampal microgliosis and astrogliosis but increased cytokine and chemokine expression in AD females. HFD-fed AD females had greater β-amyloid plaques and CAA in the thalamus compared to LFD-fed AD controls. All metrics of neuroinflammation significantly correlated with CAA pathology in the thalamus.

conclusionAD females experienced greater metabolic, cognitive, and pathologic effects in response to a HFD compared to AD males and WT controls. These observations provide a better understanding of how metabolic disease may differentially affect the development of dementia in men and women.

Indexed as

Alzheimer DiseaseCognitionDiet, High-FatSex CharacteristicsAnimalsBrainDisease Models, AnimalFemaleMaleMiceMice, TransgenicAlzheimer’s diseaseCerebral amyloid angiopathyDementiaMetabolismNeuroinflammationObesityPrediabetesSexVascularVCID

Identifiers

PMID41652508
PMCPMC12977859

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.