[Changes in microglia number and Iba1 expression level in the prefrontal cortex of type 1 diabetic mice]

Area of Science:

• Neuroscience
• Immunology
• Endocrinology

Background:

• Type 1 diabetes mellitus (T1DM) is a metabolic disorder with potential neurological complications.
• Microglia are the primary immune cells in the central nervous system and play a role in neuroinflammation.
• Disease-associated microglia (DAM) are a specific activation state linked to neurodegenerative conditions.

Purpose of the Study:

• To investigate microglial activation and the expression of DAM markers in the prefrontal cortex of T1DM mice.
• To assess the impact of T1DM on spatial learning and memory.

Main Methods:

• Induction of T1DM in C57BL/6J mice using streptozotocin (STZ).
• Evaluation of spatial learning and memory using the Morris water maze.
• Analysis of microglial activation (Iba1 expression, cell count) via immunofluorescence and Western blot.
• Quantification of DAM marker gene mRNA levels using RT-FQ-PCR.

Main Results:

• T1DM mice exhibited significantly higher fasting blood glucose and lower body weight compared to controls.
• T1DM mice showed impaired spatial learning and memory, indicated by longer escape latency in the Morris water maze.
• Increased Iba1 protein expression and a higher number of microglia were observed in the prefrontal cortex of T1DM mice.
• Significant upregulation of several DAM marker genes was detected in the prefrontal cortex of T1DM mice.

Conclusions:

• T1DM induces significant microglial activation and transformation into the DAM phenotype in the mouse prefrontal cortex.
• These neuroinflammatory changes in T1DM may contribute to cognitive deficits, specifically in spatial learning and memory.