Related Experiment Video
Updated: Apr 24, 2026

Retinal Pathophysiological Evaluation in a Rat Model
Published on: May 6, 2022
Brain aging and AD-like pathology in streptozotocin-induced diabetic rats
Jian-Qin Wang1, Jie Yin2, Yan-Feng Song2
1Nephrology Department and Blood Dialysis Center, Second Hospital of Lanzhou University, Lanzhou 730000, China.
Objective:
Numerous epidemiological studies have linked diabetes mellitus (DM) with an increased risk of developing Alzheimer's disease (AD). However, whether or not diabetic encephalopathy shows AD-like pathology remains unclear.
Research Design And Methods:
Forebrain and hippocampal volumes were measured using stereology in serial coronal sections of the brain in streptozotocin- (STZ-) induced rats. Neurodegeneration in the frontal cortex, hypothalamus, and hippocampus was evaluated using Fluoro-Jade C (FJC). Aβ aggregation in the frontal cortex and hippocampus was tested using immunohistochemistry and ELISA. Dendritic spine density in the frontal cortex and hippocampus was measured using Golgi staining, and western blot was conducted to detect the levels of synaptophysin. Cognitive ability was evaluated through the Morris water maze and inhibitory avoidant box.
Results:
Rats are characterized by insulin deficiency accompanied with polydipsia, polyphagia, polyuria, and weight loss after STZ injection. The number of FJC-positive cells significantly increased in discrete brain regions of the diabetic rats compared with the age-matched control rats. Hippocampal atrophy, Aβ aggregation, and synapse loss were observed in the diabetic rats compared with the control rats. The learning and memory of the diabetic rats decreased compared with those of the age-matched control rats.
Conclusions:
Our results suggested that aberrant metabolism induced brain aging as characterized by AD-like pathologies.
Related Concept Videos
Alzheimer Disease ll: Pathophysiology
Alzheimer Disease l: Introduction
Type II Diabetes II: Pathophysiology
Diabetic Nephropathy
Diabetic Neuropathy
Type I Diabetes II: Pathophysiology

