Abstract
Background There is a need in modern pharmacology for a representative animal model which should accurately mimic sporadic Alzheimer’s disease (sAD), the prevailing type of dementia in humans, and thus could be suitable for novel drug testing. Rats treated intracerebroventricularly with the betacytotoxic agent streptozotocin (STZ-icv), have been proposed recently as a non-transgenic sAD model which demonstrates AD-like pathology features at cognitive, neurochemical and structural level. In addition to the cognitive deficits, pathological accumulation of amyloid b (Ab) peptide is one of the neuropathological hallmarks of sAD, and a growing body of evidence suggests the involvement of insulin degrading enzyme (IDE), responsible for Ab degradation, in sAD pathophysiology. We have explored the time course of cognitive deficits and hippocampal (HPC) IDE expression in the STZ-icv rat model of sAD, and the therapeutic potential of the novel multifunctional iron-chelating drug M30 to improve these deficits.
Highlights
There is a need in modern pharmacology for a representative animal model which should accurately mimic sporadic Alzheimer’s disease, the prevailing type of dementia in humans, and could be suitable for novel drug testing
In addition to the cognitive deficits, pathological accumulation of amyloid b (Ab) peptide is one of the neuropathological hallmarks of sporadic Alzheimer’s disease (sAD), and a growing body of evidence suggests the involvement of insulin degrading enzyme (IDE), responsible for Ab degradation, in sAD pathophysiology
We have explored the time course of cognitive deficits and hippocampal (HPC) IDE expression in the STZ-icv rat model of sAD, and the therapeutic potential of the novel multifunctional iron-chelating drug M30 to improve these deficits
Summary
There is a need in modern pharmacology for a representative animal model which should accurately mimic sporadic Alzheimer’s disease (sAD), the prevailing type of dementia in humans, and could be suitable for novel drug testing. Rats treated intracerebroventricularly with the betacytotoxic agent streptozotocin (STZ-icv), have been proposed recently as a non-transgenic sAD model which demonstrates AD-like pathology features at cognitive, neurochemical and structural level. In addition to the cognitive deficits, pathological accumulation of amyloid b (Ab) peptide is one of the neuropathological hallmarks of sAD, and a growing body of evidence suggests the involvement of insulin degrading enzyme (IDE), responsible for Ab degradation, in sAD pathophysiology. We have explored the time course of cognitive deficits and hippocampal (HPC) IDE expression in the STZ-icv rat model of sAD, and the therapeutic potential of the novel multifunctional iron-chelating drug M30 to improve these deficits
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