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Brain aging and AD-like pathology in streptozotocin-induced diabetic rats.

Wang JQ, Yin J, Song YF, Zhang L, Ren YX, Wang DG, Gao LP, Jing YH - J Diabetes Res (2014)

Bottom Line: 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.Our results suggested that aberrant metabolism induced brain aging as characterized by AD-like pathologies.

View Article: PubMed Central - PubMed

Affiliation: Nephrology Department and Blood Dialysis Center, Second Hospital of Lanzhou University, Lanzhou 730000, China.

ABSTRACT

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.

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Related in: MedlinePlus

Evaluation of the cognition of diabetic rats at 4 months after STZ injection. (a) Representative traces by the Morris water maze. The performance of rats in the Morris water maze using hidden platform training for 4 d was assessed based on (b) escape latency and (c) swimming velocity in the normal and DM groups. (d) Freezing duration was measured using inhibitory avoidance box. *P < 0.05, significant difference compared with the age-matched control rats; **P < 0.01, significant difference compared with the age-matched control rats; n = 12.
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fig6: Evaluation of the cognition of diabetic rats at 4 months after STZ injection. (a) Representative traces by the Morris water maze. The performance of rats in the Morris water maze using hidden platform training for 4 d was assessed based on (b) escape latency and (c) swimming velocity in the normal and DM groups. (d) Freezing duration was measured using inhibitory avoidance box. *P < 0.05, significant difference compared with the age-matched control rats; **P < 0.01, significant difference compared with the age-matched control rats; n = 12.

Mentions: At 1 d after training, no significant difference in the time to find the platform (escape latency) was found between the diabetic rats and age-matched control rats at 4 months after STZ injection. At 2, 3, and 4 d after training, the escape latency exhibited by the diabetic rats was significantly longer than that exhibited by the control rats (Figures 6(a) and 6(b)). The velocity of swimming has no significant difference in both groups (Figure 6(c)). No significant difference in training of IA was observed between the diabetic rats and age-matched control rats at 4 months after STZ injection. However, at 24, 48, and 72 h after training, the freezing duration exhibited by the diabetic rats was notably shorter than that exhibited by the control rats (Figure 6(d)).


Brain aging and AD-like pathology in streptozotocin-induced diabetic rats.

Wang JQ, Yin J, Song YF, Zhang L, Ren YX, Wang DG, Gao LP, Jing YH - J Diabetes Res (2014)

Evaluation of the cognition of diabetic rats at 4 months after STZ injection. (a) Representative traces by the Morris water maze. The performance of rats in the Morris water maze using hidden platform training for 4 d was assessed based on (b) escape latency and (c) swimming velocity in the normal and DM groups. (d) Freezing duration was measured using inhibitory avoidance box. *P < 0.05, significant difference compared with the age-matched control rats; **P < 0.01, significant difference compared with the age-matched control rats; n = 12.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4150474&req=5

fig6: Evaluation of the cognition of diabetic rats at 4 months after STZ injection. (a) Representative traces by the Morris water maze. The performance of rats in the Morris water maze using hidden platform training for 4 d was assessed based on (b) escape latency and (c) swimming velocity in the normal and DM groups. (d) Freezing duration was measured using inhibitory avoidance box. *P < 0.05, significant difference compared with the age-matched control rats; **P < 0.01, significant difference compared with the age-matched control rats; n = 12.
Mentions: At 1 d after training, no significant difference in the time to find the platform (escape latency) was found between the diabetic rats and age-matched control rats at 4 months after STZ injection. At 2, 3, and 4 d after training, the escape latency exhibited by the diabetic rats was significantly longer than that exhibited by the control rats (Figures 6(a) and 6(b)). The velocity of swimming has no significant difference in both groups (Figure 6(c)). No significant difference in training of IA was observed between the diabetic rats and age-matched control rats at 4 months after STZ injection. However, at 24, 48, and 72 h after training, the freezing duration exhibited by the diabetic rats was notably shorter than that exhibited by the control rats (Figure 6(d)).

Bottom Line: 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.Our results suggested that aberrant metabolism induced brain aging as characterized by AD-like pathologies.

View Article: PubMed Central - PubMed

Affiliation: Nephrology Department and Blood Dialysis Center, Second Hospital of Lanzhou University, Lanzhou 730000, China.

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus