Publications by authors named "H W Katinger"

Patients with chronic pain often complain about memory impairments. Experimental studies have shown neuroprotective effects of Carbamylated erythropoietin (Cepo-Fc) in the treatment of cognitive dysfunctions. However, little is currently known about its precise molecular mechanisms in a model of inflammatory pain.

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Article Synopsis
  • - The article had an error related to the arrangement of cell images in Figure 2.
  • - The same image intended for the Aβ group was incorrectly shown for the Aβ + LY group.
  • - A corrected version of the figure is included in the article's correction.
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  • * It finds that CEPO-Fc significantly reduces cell loss and caspase-3 activation caused by Aβ and alters important signaling pathways like Akt and GSK-3β, which are linked to cell survival.
  • * The results indicate that CEPO-Fc's protective effects primarily involve the PI3K/Akt pathway rather than ERK signaling, suggesting its potential as a therapeutic agent for neurodegenerative diseases such as Alzheimer's disease.
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Intracerebroventricular (icv) administration of streptozotocin (STZ) has been used as a metabolic model of sporadic Alzheimer's disease (AD). Erythropoietin (EPO) possesses neuroprotective and memory-improving effects, which might be advantageous in treating different characteristics of AD. Nevertheless, the hematopoietic effect of EPO has hindered its application as a neuroprotective agent.

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Alzheimer's disease (AD) is a debilitating neurodegenerative disease, characterized by extracellular deposition of senile plaques, mostly amyloid β-protein (Aβ) and neuronal loss. The neuroprotective effects of erythropoietin (EPO) have been reported in some models of neurodegenerative disease, but because of its hematopoietic side effects, its derivatives lacking hematopoietic bioactivity is recommended. In this study, the neuroprotective effects of carbamylated erythropoietin-Fc (CEPO-Fc) against beta amyloid-induced memory deficit were evaluated.

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