Curcuminoids rescue long‐term potentiation impaired by amyloid peptide in rat hippocampal slices

Ahmed, Touqeer; Gilani, Anwarul Hassan; Hosseinmardi, Narges; Semnanian, Saeed; Enam, Syed Ather; Fathollahi, Yaghoub

doi:10.1002/syn.20876

Cited by 40 publications

(28 citation statements)

References 44 publications

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“…Structurally speaking, site II is less flexible than site I [24], the molecular size of Bdmc makes it easier to fit into site II than Cur. Similar relationship between curcuminoids was found by Ahmed T et al that curcuminoids rescue long-term potentiation impaired by amyloid peptide in rat hippocampal slices in the order of Bdmc > Dmc > Cur [42].…”

Section: Discussionsupporting

confidence: 83%

Differential Effects of Methoxy Group on the Interaction of Curcuminoids with Two Major Ligand Binding Sites of Human Serum Albumin

et al. 2014

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Curcuminoids are a group of compounds with a similar chemical backbone structure but containing different numbers of methoxy groups that have therapeutic potential due to their anti-inflammatory and anti-oxidant properties. They mainly bind to albumin in plasma. These findings influence their body disposition and biological activities. Spectroscopic analysis using site specific probes on human serum albumin (HSA) clearly indicated that curcumin (Cur), demethylcurcumin (Dmc) and bisdemethoxycurcumin (Bdmc) bind to both Site I (sub-site Ia and Ib) and Site II on HSA. At pH 7.4, the binding constants for Site I were relatively comparable between curcuminoids, while the binding constants for Site II at pH 7.4 were increased in order Cur < Dmc < Bdmc. Binding experiments using HSA mutants showed that Trp214 and Arg218 at Site I, and Tyr411 and Arg410 at Site II are involved in the binding of curcuminoids. The molecular docking of all curcuminoids to the Site I pocket showed that curcuminoids stacked with Phe211 and Trp214, and interacted with hydrophobic and aromatic amino acid residues. In contrast, each curcuminoid interacted with Site II in a different manner depending whether a methoxy group was present or absent. A detailed analysis of curcuminoids-albumin interactions would provide valuable information in terms of understanding the pharmacokinetics and the biological activities of this class of compounds.

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Section: Discussionsupporting

confidence: 83%

Differential Effects of Methoxy Group on the Interaction of Curcuminoids with Two Major Ligand Binding Sites of Human Serum Albumin

et al. 2014

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“…27,28 Curcuminoids can restore the capacity for plastic changes in CA1 excitability that is impaired by exposure to the Aβ peptide and rescue the reduction in long-term potentiation (LTP) in Aβ-peptideexposed hippocampal CA1 neurons. 29 We have previously reported that curcumin improves the spatial learning and memory abilities of APPswe/ PS1dE9 double transgenic mice. 23 Therefore, we sought to determine whether curcumin affects the pathology of AD via the synapses.…”

Section: Discussionmentioning

confidence: 95%

Effects of curcumin on synapses in APPswe/PS1dE9 mice

Wang

Wei

et al. 2016

Int J Immunopathol Pharmacol

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Significant losses of synapses have been demonstrated in studies of Alzheimer's disease (AD), but structural and functional changes in synapses that depend on alterations of the postsynaptic density (PSD) area occur prior to synaptic loss and play a crucial role in the pathology of AD. Evidence suggests that curcumin can ameliorate the learning and memory deficits of AD. To investigate the effects of curcumin on synapses, APPswe/PS1dE9 double transgenic mice (an AD model) were used, and the ultra-structures of synapses and synapse-associated proteins were observed. Six months after administration, few abnormal synapses were observed upon electron microscopy in the hippocampal CA1 areas of the APPswe/PS1dE9 double transgenic mice. The treatment of the mice with curcumin resulted in improvements in the quantity and structure of the synapses. Immunohistochemistry and western blot analyses revealed that the expressions of PSD95 and Shank1 were reduced in the hippocampal CA1 areas of the APPswe/PS1dE9 double transgenic mice, but curcumin treatment increased the expressions of these proteins. Our findings suggest that curcumin improved the structure and function of the synapses by regulating the synapse-related proteins PSD95 and Shank1.

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“…Curcumin can reduce amyloid in vivo in transgenic AD models and remove existing plaques [248-251]. Curcumin also reduces Aβ-mediated blockade of long-term potentiation (LTP) [252], a likely electrophysiological correlate of learning and memory. Trials of curcumin in AD patients have been explored [253] and further studies are ongoing.…”

Section: Discussionmentioning

confidence: 99%

Atherosclerosis and Alzheimer - diseases with a common cause? Inflammation, oxysterols, vasculature

2014

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BackgroundAging is accompanied by increasing vulnerability to pathologies such as atherosclerosis (ATH) and Alzheimer disease (AD). Are these different pathologies, or different presentations with a similar underlying pathoetiology?DiscussionBoth ATH and AD involve inflammation, macrophage infiltration, and occlusion of the vasculature. Allelic variants in common genes including APOE predispose to both diseases. In both there is strong evidence of disease association with viral and bacterial pathogens including herpes simplex and Chlamydophila. Furthermore, ablation of components of the immune system (or of bone marrow-derived macrophages alone) in animal models restricts disease development in both cases, arguing that both are accentuated by inflammatory/immune pathways. We discuss that amyloid β, a distinguishing feature of AD, also plays a key role in ATH. Several drugs, at least in mouse models, are effective in preventing the development of both ATH and AD. Given similar age-dependence, genetic underpinnings, involvement of the vasculature, association with infection, Aβ involvement, the central role of macrophages, and drug overlap, we conclude that the two conditions reflect different manifestations of a common pathoetiology.MechanismInfection and inflammation selectively induce the expression of cholesterol 25-hydroxylase (CH25H). Acutely, the production of ‘immunosterol’ 25-hydroxycholesterol (25OHC) defends against enveloped viruses. We present evidence that chronic macrophage CH25H upregulation leads to catalyzed esterification of sterols via 25OHC-driven allosteric activation of ACAT (acyl-CoA cholesterol acyltransferase/SOAT), intracellular accumulation of cholesteryl esters and lipid droplets, vascular occlusion, and overt disease.SummaryWe postulate that AD and ATH are both caused by chronic immunologic challenge that induces CH25H expression and protection against particular infectious agents, but at the expense of longer-term pathology.

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Curcuminoids rescue long‐term potentiation impaired by amyloid peptide in rat hippocampal slices

Cited by 40 publications

References 44 publications

Differential Effects of Methoxy Group on the Interaction of Curcuminoids with Two Major Ligand Binding Sites of Human Serum Albumin

Differential Effects of Methoxy Group on the Interaction of Curcuminoids with Two Major Ligand Binding Sites of Human Serum Albumin

Effects of curcumin on synapses in APPswe/PS1dE9 mice

Atherosclerosis and Alzheimer - diseases with a common cause? Inflammation, oxysterols, vasculature

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