ArticleNeurochemical research2025
Multidimensional Evaluation of the Streptozotocin-Induced Alzheimer's Model: Integrating Molecular, Histopathological, and Behavioral Correlates Over Time.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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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.
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Who cites it
1 citing paper in PubMed.
- Vitamin DInternational journal of molecular sciences · 2026Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized by cognitive deterioration, oxidative stress and neuroinflammation. Reliable preclinical models for sporadic AD are lacking. The intracerebroventricular (ICV) streptozotocin (STZ) model simulates pathology of sporadic AD; its timeline remains ambiguous. We assessed multiple endpoints in male Wistar rats 1 and 3 months post-ICV STZ (3 mg/kg; n = 72; control, sham, STZ). Spatial and associative memory was tested via the Morris Water Maze and Passive Avoidance Task. Hippocampal superoxide dismutase (SOD), tumor necrosis factor-α (TNF-α), and brain-derived neurotrophic factor (BDNF) were measured by ELISA; neuronal integrity and amyloid deposits by hematoxylin-eosin (H&E) and Congo red staining. STZ groups (3-months vs. 1-month) exhibited cognitive deficits: increased escape latency (80.14 ± 5.75 vs. 65.68 ± 11.51 s; P = 0.008), decreased time in the target quadrant (7.32 ± 0.71 vs. 11.6 ± 1.99 s; P = 0.019), platform crossings (0.83 ± 0.4 vs. 2.5 ± 0.83; P < 0.001) and step-through latency (3.89 ± 1.14 vs. 12.43 ± 3.28 s; P = 0.011). SOD activity decreased (6.28 ± 0.76 vs. 10.11 ± 1.26 U/mg; P = 0.015), TNF-α increased (71.17 ± 2.16 vs. 58.06 ± 2.22 pg/mg; P = 0.004) and BDNF declined (47.09 ± 9.21 vs. 86.83 ± 8.51 pg/mg; P < 0.001). Histology revealed neuronal shrinkage, vacuolation and amyloid deposits in 3-months STZ rats. The ICV STZ model recapitulates AD features: cognitive decline, oxidative stress, neuroinflammation and compromised neurotrophic support. Limitations such as lack of neurofibrillary tangles and sex evaluations require investigation. Studies exploring tau pathology, sex differences, and long-term dynamics may refine therapeutic strategies.
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Registered trials
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 OpenQuestion graph.