Type 1 diabetes

Alterations in gray matter structure associated with cognitive decline in T1DM mice (T1DM) patients and mice: A voxel-based morphometry study

Diabetes Res Clin PractPublished Cross-sectional study

Authors' conclusion

The GM volumes of cerebellar lobules were associated with cognitive scores in T1DM patients, suggesting that GM structural alterations in these lobules may be involved in the neuropathological mechanisms of brain damage in T1DM. And the GM atrophy in T1DM mice confirmed those changes in T1DM patients and provided valuable information for identifying potential vulnerable brain areas associated with cognitive decline in T1DM.

Study context

Population
Adults with T1D and healthy controls; T1D mice and normal control miceT1D mice 24 · normal control mice 12
Participants
73 adults
Exposure
T1D vs healthy controls; T1D mice vs normal control mice
Outcome
GM volume (Voxel-based Morphometry (VBM), structural magnetic resonance imaging (MRI))
Methodological detailsvoxel-based morphometry, clinical study and animal experiment
  • Voxel-based morphometry
  • Clinical study and animal experiment

Main finding

As reported in the abstract

  • Significant decrease in gray matter (GM) volume of the right cerebellar Crus I in T1DM patients vs healthy controls (HCs)
  • GM volumes of cerebellar lobules closely related to cognitive scores and serum lipid levels in T1DM patients

Observational data: associations, not effects.

Further findings

GM atrophy in mice (T1DM, n = 24 vs NC, n = 12)

Brain regions with GM atrophy in T1DM vs NC mice, incl. cerebellum, prefrontal cortex
23

Parts of this Brief are withheld: the automatic checks could not confirm them against the abstract.

Original publication

Alterations in gray matter structure associated with cognitive decline in T1DM patients and mice: A voxel-based morphometry study. Diabetes Res Clin Pract. Published 7 April 2026. doi:10.1016/j.diabres.2026.113252

Composed by AI from the published abstract and checked against it. How Briefs are made →

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