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

Sil, Susmita; Ghosh, Tusharkanti

doi:10.1016/j.jneuroim.2015.12.003

Cited by 66 publications

(37 citation statements)

References 29 publications

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“…ICV colchicine triggers neuro-infammatory changes in brain, enhance COX-2, TNF-α and other pro-inflammatory cytokine production (35). In the present study the brain TNF-α content of colchicine treated rats was greatly enhanced in comparison to the sham control rats.…”

Section: Discussionsupporting

confidence: 48%

Ellagic Acid Administration Reverses Colchicine- Induced Dementia in Rats

Kaur¹,

Kumar²,

Bansal³

2016

JPTRM

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The late-onset sporadic type of Alzheimer's disease is characterised by chronic oxidative stress, neuroinflammation and cognitive dysfunction. Ellagic acid is a naturally occurring polyphenol known to possess robust antioxidant property. In the present study, memory enhancing potential of ellagic acid has been explored against ICV colchicine induced dementia in rats. Colchicine (15µg/rat) was administered to Wistar rats (200g) through intracerebroventricular (ICV) route by using stereotaxic apparatus. ICV colchicine induces Alzheimer's disease like changes in the brain such as rampant free radical production, neuroinflammation and selective neurodegeneration in hippocampus and cortex by acting as an antitubulin agent (mitotic poison). Ellagic acid (17.5 and 35 mg/kg, p.o.) was administered to rats for 25 successive days. Morris water maze and elevated plus maze paradigms were utilized to assess the spatial memory of rats. Oxidative stress biomarkers along with TNF-α were also measured in brain of rats. Ellagic acid prevented the ICV colchicine triggered cognitive deficits as evident by a significant (p<0.05) reduction in mean escape latency during acquisition trial and increased (p<0.05) time spent in target quadrant during probe trial in Morris water maze test, and reduction (p<0.05) in transfer latency in elevated plus maze test. Furthermore, both the doses of ellagic acid attenuated ICV colchicine induced rise in brain TBARS as well as TNF-α and simultaneously enhanced the GSH content.

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Section: Discussionsupporting

confidence: 48%

Ellagic Acid Administration Reverses Colchicine- Induced Dementia in Rats

Kaur¹,

Kumar²,

Bansal³

2016

JPTRM

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“…Aging and oxidative stress are associated with declines in hippocampal processing of information [6–8] as demonstrated by the deficits seen in spatial learning, memory formation, and the decline in long term potentiation that is necessary for memory consolidation. Multiple reports have identified a correlation between COX-2 expression, reduction in eicosanoid production, systemic inflammation (i.e., TNF α , MIP1- α , and IL-1 β expression), and the pathogenesis of AD leading to loss in memory and speed of information processing in specific animal models [9, 10]. The protective effect of nonspecific anti-inflammatory drugs (NSAIDs) in the pathogenesis of AD is attributed to COX-2 inhibition and the direct prevention of amyloid plaque accumulation in the brain.…”

Section: Introductionmentioning

confidence: 99%

Clinical and Preclinical Cognitive Function Improvement after Oral Treatment of a Botanical Composition Composed of Extracts fromScutellaria baicalensisandAcacia catechu

Yimam

Burnett²,

Brownell

et al. 2016

Behavioural Neurology

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Dementia and cognitive impairment have become the major concerns worldwide due to a significantly aging population, increasing life span and lack of effective pharmacotherapy. In light of limited pharmaceutical drug choices and the socioeconomic implications of these conditions, the search for safe and effective alternatives from natural sources has gained many attractions within the medical food and dietary supplement industry. Two polyphenol extracts derived from roots of Scutellaria baicalensis and heartwoods of Acacia catechu containing free-B-ring flavonoids and flavans, respectively, were combined into a proprietary blend called UP326. A similar bioflavonoid composition, UP446, has been reported with modulation of pathways related to systemic inflammation. To test the effect of UP326 on memory and learning, a radial arm water maze (RAWM) and contextual fear conditioning (CF) were utilized in aged F344 rats fed with UP326 at doses of 3, 7, and 34 mg/kg for 11 weeks. The 7 and 34 mg/kg dosage groups had significantly fewer errors than aged vehicle control animals and their performance was equivalent to young animal controls. In a separate human clinical trial, test subjects orally given 300 mg of UP326 BID for 30 days showed marked improvement in speed and accuracy of processing complex information in computer tasks and reduced their standard deviation of performance compared to baseline and the placebo group. This data suggest that UP326 may help maintain memory, sustain speed of processing, and reduce the number or memory errors as we age.

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“…Neuroinflammation is both a contributing factor to and a consequence of neurodegeneration and contributes to cognitive dysfunction (Cunningham et al 2009; Sil and Ghosh 2016; Singhal et al 2014). It has been suggested that chronic inflammation in response to neuronal damage may accelerate and potentially underlie disease progression in AD, with resident microglia being a key player involved in neuronal and synaptic loss.…”

Section: Introductionmentioning

confidence: 99%

Modulation of neuroinflammation and pathology in the 5XFAD mouse model of Alzheimer's disease using a biased and selective beta-1 adrenergic receptor partial agonist

Ardestani

Evans

et al. 2017

Neuropharmacology

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Degeneration of noradrenergic neurons occurs at an early stage of Alzheimer’s Disease (AD). The noradrenergic system regulates arousal and learning and memory, and has been implicated in regulating neuroinflammation. Loss of noradrenergic tone may underlie AD progression at many levels. We have previously shown that acute administration of a partial agonist of the beta-1 adrenergic receptor (ADRB1), xamoterol, restores behavioral deficits in a mouse model of AD. The current studies examined the effects of chronic low dose xamoterol on neuroinflammation, pathology, and behavior in the pathologically aggressive 5XFAD transgenic mouse model of AD. In vitro experiments in cells expressing human beta adrenergic receptors demonstrate that xamoterol is highly selective for ADRB1 and functionally biased for the cAMP over the β-arrestin pathway. Data demonstrate ADRB1-mediated attenuation of TNF-α production with xamoterol in primary rat microglia culture following LPS challenge. Finally, two independent cohorts of 5XFAD and control mice were administered xamoterol from approximately 4.0–6.5 or 7.0–9.5 months, were tested in an array of behavioral tasks, and brains were examined for evidence of neuroinflammation, and amyloid beta and tau pathology. Xamoterol reduced mRNA expression of neuroinflammatory markers (Iba1, CD74, CD14 and TGFβ) and immunohistochemical evidence for microgliosis and astrogliosis. Xamoterol reduced amyloid beta and tau pathology as measured by regional immunohistochemistry. Behavioral deficits were not observed for 5XFAD mice. In conclusion, chronic administration of a selective, functionally biased, partial agonist of ADRB1 is effective in reducing neuroinflammation and amyloid beta and tau pathology in the 5XFAD model of AD.

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

Cited by 66 publications

References 29 publications

Ellagic Acid Administration Reverses Colchicine- Induced Dementia in Rats

Ellagic Acid Administration Reverses Colchicine- Induced Dementia in Rats

Clinical and Preclinical Cognitive Function Improvement after Oral Treatment of a Botanical Composition Composed of Extracts fromScutellaria baicalensisandAcacia catechu

Modulation of neuroinflammation and pathology in the 5XFAD mouse model of Alzheimer's disease using a biased and selective beta-1 adrenergic receptor partial agonist

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