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    <subfield code="a">Possible modulatory effect of tadalafil and bergapten on experimentally induced cognitive impairment in mice / </subfield>
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    <subfield code="a">Sporadic Alzheimer{u2019}s disease (SAD) is a slowly progressive neurodegenerative disorder characterized by deposition of amyloid beta (A&#xDD;) plaques, tau protein aggregation, impaired insulin signaling, and neuroinflammation. This study aimed to investigate the neuroprotective potential of tadalafil (TAD) and bergapten (BG) in SAD-induced cognitive impairment in mice. SAD was induced by a single intracerebroventricular injection of streptozotocin (STZ) (3 mg/kg). TAD or BG was administered intraperitoneally at doses of 20 and 25 mg/kg, respectively, 5 hours after STZ injection for 21 consecutive days. TAD and BG conceivably attenuated STZ-induced hippocampal insult, preserved neuronal integrity, and improved cognitive function in the Morris water maze and object recognition tests paralleled by reduced A&#xDD; expression and phosphorylation of tau. Moreover, TAD and BG enhanced the protein expression of pAkt, pGSK-3&#xDD;, beclin-1, and methylated protein phosphatase 2A (PP2A) and cyclin D1 gene expression and raised brain-derived neurotrophic factor immunoreactivity. In addition, both drugs boosted the hippocampal levels of cyclic guanosine monophosphate (cGMP), protein kinase G (PKG), WNT3A, and adenosine monophosphate-activated protein kinase coupled by reduced protein expression of &#xDD;-catenin and mammalian target of rapamycin (mTOR). TAD and BG also halted neuroinflammation as evidenced by reduced IL-23 and IL-27 levels and NF-mB protein expression</subfield>
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