Introduction: Metabolic dysfunctions are critical in the pathology
of Alzheimer’s disease. Impaired zinc homeostasis, in particular, is
a significant issue in this disease that has yet to be explained. Gene
expression of ZIP14 in brain tissue has been previously reported.
But to date, only one study has reported reduced ZIP14 levels in
aged brain tissue. We investigated how dietary zinc deprivation and
supplementation impact ZIP14 levels in the cerebral cortex in rats with
sporadic Alzheimer’s disease (sAH) produced by intracerebroventricular
streptozotocin (icv-STZ). Impaired zinc homeostasis, in particular, is a
significant issue with this condition that has yet to be elucidated.
Methods: Animals were divided into 5 groups in equal numbers (n=8):
Sham 1 group: icv received artificial cerebrospinal fluid (aCSF); Sham
2 group: retrieved icv aCSF and intraperitoneal (ip) saline, STZ group:
received 3 mg/kg icv-STZ; STZ-Zn-Deficient group: received 3 mg/
kg icv-STZ and fed a zinc-deprived diet; STZ-Zn-Supplemented: It
received 3 mg/kg icv-STZ and ip zinc sulfate (5 mg/kg/day ZIP 14 levels
(ng/L) in cortex tissue samples taken from animals sacrificed under
general anesthesia were determined by ELISA at the final stage of the
experimental applications.
Results: Decreased ZIP14 levels in the sporadic Alzheimer’s group were
severely by zinc deficiency. Zinc supplementation treated the reduction
in ZIP14 levels.
Conclusion: The results of the current study show that ZIP14 levels in
cerebral cortex tissue, which are suppressed in the experimental rat
Alzheimer model and are even more critically reduced in zinc deficiency,
can be restored by zinc supplementation.
Keywords: Cerebral cortex, icv-STZ Injection, ZIP14, zinc deficiency, zinc
supplementation