Research Article

Investigation of the Relationship Between Neurogenesis and Metabolic Parameters in the Streptozotocin-Induced Alzheimer’s Disease Model

Number: 1 March 1, 2026
TR EN

Investigation of the Relationship Between Neurogenesis and Metabolic Parameters in the Streptozotocin-Induced Alzheimer’s Disease Model

Abstract

Aim: In this study, we aimed to analyze the interactions between neuroplasticity-related proteins (DCX, EGR1, sFRP3) and metabolic markers (insulin, HbA1c, asprosin) in an STZ-induced Alzheimer's disease model, as well as to evaluate how changes in these parameters affect the pathophysiology of Alzheimer's disease (AD). Material and Methods: 14 male Wistar albino rats, aged 8 to 10 weeks, weighing 250–300 g, were used. The animals were divided into two groups: control and Alzheimer's model. The AD model was created by stereotaxic injection of STZ, and the control group was injected with artificial CSF. The animals were monitored for 14 days after surgery. At the end of the study, serum samples were collected and DCX, EGR1, sFRP3, insulin, gHbA1c, and asprosin levels were analyzed by ELISA. The variables were compared between the groups, and P-values < 0.05 were considered significant. Results: DCX and EGR1 levels showed borderline changes without statistical significance (p = 0.056 and p = 0.080, respectively), while sFRP3 levels were significantly higher in the AD group (p = 0.012). Insulin levels did not differ (p = 0.829), but asprosin and gHbA1c levels were significantly higher (p = 0.046 and p = 0.000, respectively), indicating metabolic derangement. Correlation analysis showed strong positive correlations between asprosin and gHbA1c (r = 0.807, p < 0.01) and sFRP3 and EGR1 (r = 0.780, p < 0.01), suggesting interconnected roles in AD pathophysiology. Conclusion: This study shows the relationship between neurogenesis and metabolic parameters in AD.

Keywords

Supporting Institution

None

Ethical Statement

Animal experiments were approved by the Dicle University Experimental Animals Local Ethics Committee (HADYEK) (Ethical approval no: 04, date: 26/12/2024).

Thanks

None

References

  1. Breijyeh Z, Karaman R. Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules. 2020 Dec 8;25(24):5789. doi: 10.3390/molecules25245789.
  2. Wijesekara N, Ahrens R, Sabale M, Wu L, Ha K, Verdile G, Fraser PE. Amyloid-β and islet amyloid pathologies link Alzheimer’s disease and type 2 diabetes in a transgenic model. FASEB J. 2017 Dec;31(12):5409-5418. doi: 10.1096/fj.201700431R.
  3. Ezkurdia A, Ramírez MJ, Solas M. Metabolic Syndrome as a Risk Factor for Alzheimer’s Disease: A Focus on Insulin Resistance. Int J Mol Sci. 2023 Feb 22;24(5):4354. doi: 10.3390/ijms24054354.
  4. Razay G, Vreugdenhil A, Wilcock G. The metabolic syndrome and Alzheimer disease. Arch Neurol. 2007 Jan;64(1):93-6. doi: 10.1001/archneur.64.1.93.
  5. Arendt T. Synaptic plasticity and cell cycle activation in neurons are alternative effector pathways: the, dr.jekyll and mr. Hyde concept of Alzheimer’s disease or the yin and yang of neurolasticity. Prog Neurobiol 2003;71(2-3):83-248
  6. Turrigiano GG, Nelson SB. Hebb and homeostasis in neuronal plasticity. Curr Opin Neurobiol 2000;10 (3):358-364
  7. Manohar S, Paolone NA, Bleichfeld M, Hayes SH, Salvi RJ, Baizer JS. Expression of doublecortin, a neuronal migration protein, in unipolar brush cells of the vestibulocerebellum and dorsal cochlear nucleus of the adult rat. Neuroscience. 2012;202:169-183. doi:10.1016/j.neuroscience.2011.12.013
  8. Duclot F, Kabbaj M. The Role of Early Growth Response 1 (EGR1) in Brain Plasticity and Neuropsychiatric Disorders. Front Behav Neurosci. 2017 Mar 6;11:35. doi: 10.3389/fnbeh.2017.

Details

Primary Language

English

Subjects

Neurology and Neuromuscular Diseases, Physiopathology

Journal Section

Research Article

Publication Date

March 1, 2026

Submission Date

June 14, 2025

Acceptance Date

July 28, 2025

Published in Issue

Year 2026 Number: 1

APA
Gökdemir, G. Ş., & Yokuş, B. (2026). Investigation of the Relationship Between Neurogenesis and Metabolic Parameters in the Streptozotocin-Induced Alzheimer’s Disease Model. Medical Records, 1. https://doi.org/10.37990/medr.1719633
AMA
1.Gökdemir GŞ, Yokuş B. Investigation of the Relationship Between Neurogenesis and Metabolic Parameters in the Streptozotocin-Induced Alzheimer’s Disease Model. Med Records. 2026;(1). doi:10.37990/medr.1719633
Chicago
Gökdemir, Gül Şahika, and Beran Yokuş. 2026. “Investigation of the Relationship Between Neurogenesis and Metabolic Parameters in the Streptozotocin-Induced Alzheimer’s Disease Model”. Medical Records, no. 1. https://doi.org/10.37990/medr.1719633.
EndNote
Gökdemir GŞ, Yokuş B (March 1, 2026) Investigation of the Relationship Between Neurogenesis and Metabolic Parameters in the Streptozotocin-Induced Alzheimer’s Disease Model. Medical Records 1
IEEE
[1]G. Ş. Gökdemir and B. Yokuş, “Investigation of the Relationship Between Neurogenesis and Metabolic Parameters in the Streptozotocin-Induced Alzheimer’s Disease Model”, Med Records, no. 1, Mar. 2026, doi: 10.37990/medr.1719633.
ISNAD
Gökdemir, Gül Şahika - Yokuş, Beran. “Investigation of the Relationship Between Neurogenesis and Metabolic Parameters in the Streptozotocin-Induced Alzheimer’s Disease Model”. Medical Records. 1 (March 1, 2026). https://doi.org/10.37990/medr.1719633.
JAMA
1.Gökdemir GŞ, Yokuş B. Investigation of the Relationship Between Neurogenesis and Metabolic Parameters in the Streptozotocin-Induced Alzheimer’s Disease Model. Med Records. 2026. doi:10.37990/medr.1719633.
MLA
Gökdemir, Gül Şahika, and Beran Yokuş. “Investigation of the Relationship Between Neurogenesis and Metabolic Parameters in the Streptozotocin-Induced Alzheimer’s Disease Model”. Medical Records, no. 1, Mar. 2026, doi:10.37990/medr.1719633.
Vancouver
1.Gül Şahika Gökdemir, Beran Yokuş. Investigation of the Relationship Between Neurogenesis and Metabolic Parameters in the Streptozotocin-Induced Alzheimer’s Disease Model. Med Records. 2026 Mar. 1;(1). doi:10.37990/medr.1719633