Effects of naproxen on immune responses in a colchicine-induced rat model of Alzheimer's disease.

doi:10.1159/000357735

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Effects of naproxen on immune responses in a colchicine-induced rat model of Alzheimer's disease.

Journal Article•DOI•

Effects of naproxen on immune responses in a colchicine-induced rat model of Alzheimer's disease.

Susmita Sil¹, Ananda Raj Goswami, Goutam Dutta, Tusharkanti Ghosh•Institutions (1)

University of Calcutta¹

21 Mar 2014-Neuroimmunomodulation (Karger Publishers)-Vol. 21, Iss: 6, pp 304-321

TL;DR: In this article, the components of the immune system have been indicated to be linked with the neurotoxicity in Alzheimer's disease (AD), and the participation of the immune system has been investigated.

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Abstract: Background: The components of the immune system have been indicated to be linked with the neurotoxicity in Alzheimer's disease (AD). The participation of the immu

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Journal Article•DOI•

Rodent models of neuroinflammation for Alzheimer’s disease

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Amir Nazem¹, Roman Sankowski¹, Michael Bacher², Yousef Al-Abed¹•Institutions (2)

The Feinstein Institute for Medical Research¹, University of Marburg²

17 Apr 2015-Journal of Neuroinflammation

TL;DR: Among these models, streptozotocin, PolyI:C-induced, and p25 neuroinflammation models are compatible with the inflammation hypothesis of Alzheimer’s disease.

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Abstract: Alzheimer’s disease remains incurable, and the failures of current disease-modifying strategies for Alzheimer’s disease could be attributed to a lack of in vivo models that recapitulate the underlying etiology of late-onset Alzheimer’s disease. The etiology of late-onset Alzheimer’s disease is not based on mutations related to amyloid-β (Aβ) or tau production which are currently the basis of in vivo models of Alzheimer’s disease. It has recently been suggested that mechanisms like chronic neuroinflammation may occur prior to amyloid-β and tau pathologies in late-onset Alzheimer’s disease. The aim of this study is to analyze the characteristics of rodent models of neuroinflammation in late-onset Alzheimer’s disease. Our search criteria were based on characteristics of an idealistic disease model that should recapitulate causes, symptoms, and lesions in a chronological order similar to the actual disease. Therefore, a model based on the inflammation hypothesis of late-onset Alzheimer’s disease should include the following features: (i) primary chronic neuroinflammation, (ii) manifestations of memory and cognitive impairment, and (iii) late development of tau and Aβ pathologies. The following models fit the pre-defined criteria: lipopolysaccharide- and PolyI:C-induced models of immune challenge; streptozotocin-, okadaic acid-, and colchicine neurotoxin-induced neuroinflammation models, as well as interleukin-1β, anti-nerve growth factor and p25 transgenic models. Among these models, streptozotocin, PolyI:C-induced, and p25 neuroinflammation models are compatible with the inflammation hypothesis of Alzheimer’s disease.

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187 citations

Cites background or result from "Effects of naproxen on immune respo..."

...Likewise, the nitrite level and the ROS level of hippocampus were also significantly higher in colchicine-induced neurodegeneration compared to controls and sham-operated rats [117]....
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...of AD-like neurodegeneration in this model [113,116,117]....
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...demonstrated that colchicine-induced neurodegeneration is mediated by COX-induced neuroinflammation [117]....
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...ICV-colchicine Inhibition of tubulin formation/ microtubule breakdown ? (Tau dephosphorylation) ? (Amyloid plaque) Spatial memory (14d to 21d) S1L0C1 [113] [117]...
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...It is noteworthy that naproxen administration (doses 5, 10, or 20 mg/kg) could prevent from TNF-α increase and reduce the amyloid plaque formation [117]....
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Journal Article•DOI•

Role of cox-2 mediated neuroinflammation on the neurodegeneration and cognitive impairments in colchicine induced rat model of Alzheimer's Disease.

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Susmita Sil¹, Tusharkanti Ghosh¹•Institutions (1)

University of Calcutta¹

15 Feb 2016-Journal of Neuroimmunology

TL;DR: It was showed that the impairments of memory and neurodegeneration in the hippocampus of cAD in 21-day study are mediated by cox-2 induced neuroinflammation.

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53 citations

Cites background from "Effects of naproxen on immune respo..."

...…resulted in progressive impairment of memory and neurodegeneration which were characterized as sporadic model of Alzheimer's Disease (AD) (Emerich and Walsh, 1990; Bensimon and Chermat, 1991; Shigematsu and McGeer, 1992; Kumar et al., 2006, 2007; Pitchaimani et al., 2012; Sil et al., 2014, 2015)....
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Journal Article•DOI•

Dual Role of Vitamin C on the Neuroinflammation Mediated Neurodegeneration and Memory Impairments in Colchicine Induced Rat Model of Alzheimer Disease

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Susmita Sil¹, Susmita Sil², Tusharkanti Ghosh¹, Pritha Gupta¹, Rupsa Ghosh¹, Syed N. Kabir³, Avishek Roy¹ - Show less +3 more•Institutions (3)

University of Calcutta¹, Durham University², Indian Institute of Chemical Biology³

24 Sep 2016-Journal of Molecular Neuroscience

TL;DR: The present study showed that ROS played an important role in the colchicine induced neuroinflammation linked neurodegeneration and memory impairments along with alteration of peripheral immune responses in cAD, and it also appears from the results that vitamin C at lower doses showed anti-oxidant effect and at higher dose resulted in pro-OXidant effects in c AD.

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Abstract: The neurodegeneration in colchicine induced AD rats (cAD) is mediated by cox-2 linked neuroinflammation. The importance of ROS in the inflammatory process in cAD has not been identified, which may be deciphered by blocking oxidative stress in this model by a well-known anti-oxidant vitamin C. Therefore, the present study was designed to investigate the role of vitamin C on colchicine induced oxidative stress linked neuroinflammation mediated neurodegeneration and memory impairments along with peripheral immune responses in cAD. The impairments of working and reference memory were associated with neuroinflammation and neurodegeneration in the hippocampus of cAD. Administration of vitamin C (200 and 400 mg/kg BW) in cAD resulted in recovery of memory impairments, with prevention of neurodegeneration and neuroinflammation in the hippocampus. The neuroinflammation in the hippocampus also influenced the peripheral immune responses and inflammation in the serum of cAD and all of these parameters were also recovered at 200 and 400 mg dose of vitamin C. However, cAD treated with 600 mg dose did not recover but resulted in increase of memory impairments, neurodegeneration and neuroinflammation in hippocampus along with alteration of peripheral immune responses in comparison to cAD of the present study. Therefore, the present study showed that ROS played an important role in the colchicine induced neuroinflammation linked neurodegeneration and memory impairments along with alteration of peripheral immune responses. It also appears from the results that vitamin C at lower doses showed anti-oxidant effect and at higher dose resulted in pro-oxidant effects in cAD.

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47 citations

Cites background from "Effects of naproxen on immune respo..."

...…linked with oxidative stress (OS) was not only involved with the process of neurodegeneration but it altered some peripheral immune parameters, probably by transmitting inflammatory signals through blood brain barrier (BBB) to the periphery (Britschgi and Wyss-Coray 2007; Sil et al. 2014, 2016b)....
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...Intracerebroventricular injection of colchicine in rats has been considered by several authors as amodel of sporadic dementia of Alzheimer’s type (Emerich and Walsh 1990; Bensimon and Chermat 1991;Shigematsu and McGeer 1992; Kumar et al. 2006, 2007; Pitchaimani et al. 2012; Sil et al. 2014; Sil and Ghosh 2016)....
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...…injection of colchicine in rats has been considered by several authors as amodel of sporadic dementia of Alzheimer’s type (Emerich and Walsh 1990; Bensimon and Chermat 1991;Shigematsu and McGeer 1992; Kumar et al. 2006, 2007; Pitchaimani et al. 2012; Sil et al. 2014; Sil and Ghosh 2016)....
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Book•

Proteins and nucleic acids

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Abraham Marcus

01 Jan 1981

44 citations

Journal Article•DOI•

Neuroinflammation in neurological disorders: pharmacotherapeutic targets from bench to bedside.

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Awanish Mishra¹, Ritam Bandopadhyay¹, Prabhakar Kumar Singh¹, Pragya Shakti Mishra², Neha Sharma¹, Navneet Khurana¹ - Show less +2 more•Institutions (2)

Lovely Professional University¹, Sanjay Gandhi Post Graduate Institute of Medical Sciences²

13 Aug 2021-Metabolic Brain Disease

TL;DR: In this article, a review focusing on the recent advancement in understanding molecular mechanisms of neuroinflammation and its role in the etiopathogenesis of various neurological disorders, especially Alzheimer's disease (AD), Parkinson disease (PD), and Epilepsy, is presented.

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Abstract: Neuroinflammation is one of the host defensive mechanisms through which the nervous system protects itself from pathogenic and or infectious insults. Moreover, neuroinflammation occurs as one of the most common pathological outcomes in various neurological disorders, makes it the promising target. The present review focuses on elaborating the recent advancement in understanding molecular mechanisms of neuroinflammation and its role in the etiopathogenesis of various neurological disorders, especially Alzheimer's disease (AD), Parkinson's disease (PD), and Epilepsy. Furthermore, the current status of anti-inflammatory agents in neurological diseases has been summarized in light of different preclinical and clinical studies. Finally, possible limitations and future directions for the effective use of anti-inflammatory agents in neurological disorders have been discussed.

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41 citations

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Protein Measurement with the Folin Phenol Reagent

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Oliver H. Lowry¹, Nira J. Rosebrough¹, A. Lewis Farr¹, Rose J. Randall¹•Institutions (1)

Washington University in St. Louis¹

01 Nov 1951-Journal of Biological Chemistry

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George Paxinos, Charles Watson

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TL;DR: This paper presents a meta-analyses of the determinants of earthquake-triggered landsliding in the Czech Republic over a period of 18 months in order to establish a probabilistic framework for estimating the intensity of the earthquake.

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Abstract: Preface. Acknowledgements. Introduction. References. List of Structures. Index of Abbreviations. Diagrams.

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The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics

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John Hardy¹, Dennis J. Selkoe²•Institutions (2)

National Institutes of Health¹, Brigham and Women's Hospital²

19 Jul 2002-Science

TL;DR: It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid β-peptide in plaques in brain tissue and the rest of the disease process is proposed to result from an imbalance between Aβ production and Aβ clearance.

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Abstract: It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer9s disease (AD) may be caused by deposition of amyloid β-peptide (Aβ) in plaques in brain tissue. According to the amyloid hypothesis, accumulation of Aβ in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Aβ production and Aβ clearance.

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Analysis of nitrate, nitrite, and [15N]nitrate in biological fluids

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Laura C. Green¹, David A. Wagner¹, Joseph A. Glogowski¹, Paul L. Skipper¹, John S. Wishnok¹, Steven R. Tannenbaum¹ - Show less +2 more•Institutions (1)

Massachusetts Institute of Technology¹

01 Oct 1982-Analytical Biochemistry

TL;DR: A new automated system for the analysis of nitrate via reduction with a high-pressure cadmium column that automatically eliminates interference from other compounds normally present in urine and other biological fluids is described.

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Curcumin Inhibits Formation of Amyloid β Oligomers and Fibrils, Binds Plaques, and Reduces Amyloid in Vivo

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Fusheng Yang¹, Giselle P. Lim², Giselle P. Lim¹, Aynun N. Begum¹, Aynun N. Begum², Oliver J. Ubeda², Oliver J. Ubeda¹, Mychica Simmons², Mychica Simmons¹, Surendra S. Ambegaokar¹, Surendra S. Ambegaokar², Pingping P. Chen¹, Pingping P. Chen², Rakez Kayed³, Charles G. Glabe³, Sally A. Frautschy¹, Sally A. Frautschy², Gregory M. Cole², Gregory M. Cole¹ - Show less +15 more•Institutions (3)

University of California, Los Angeles¹, Veterans Health Administration², University of California, Irvine³

18 Feb 2005-Journal of Biological Chemistry

TL;DR: It is suggested that low dose curcumin effectively disaggregates Aβ as well as prevents fibril and oligomer formation, supporting the rationale forCurcumin use in clinical trials preventing or treating AD.

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2,140 citations