Inflammation in neurodegenerative diseases

Amor, Sandra; Puentes, Fabìola; Baker, David; Valk, Paul van der

doi:10.1111/j.1365-2567.2009.03225.x

Cited by 1,174 publications

(886 citation statements)

References 115 publications

(200 reference statements)

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“…Pathways transduced by the activation of TNF receptor-1 are linked to the induced expression of COX-2 [23] . Furthermore, these cytokines may stimulate the expression of [24] . This process may lead to the production of toxic amounts of NO free radicals, which in turn could potentiate the expression and release of TNF-α by adjacent microglial cells and thereby further amplify the inflammatory reaction [15,25] .…”

Section: Discussionmentioning

confidence: 99%

6-Shogaol, an active compound of ginger, protects dopaminergic neurons in Parkinson's disease models via anti-neuroinflammation

Park

Kim

et al. 2013

Acta Pharmacol Sin

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Aim: 6-Shogaol [1-(4-hydroxy-methoxyphenyl)-4-decen-one], a pungent compound isolated from ginger, has shown various neurobiological and anti-inflammatory effects. The aim of this study was to examine the effects of 6-shogaol on neuroinflammatory-induced damage of dopaminergic (DA) neurons in Parkinson's disease (PD) models. Methods: Cultured rat mesencephalic cells were treated with 6-shogaol (0.001 and 0.01 μmol/L) for 1 h, then with MPP + (10 µmol/L) for another 23 h. The levels of TNF-α and NO in medium were analyzed spectrophotometrically. C57/BL mice were administered 6-shogaol (10 mg·kg -1 ·d -1 , po) for 3 d, and then MPTP (30 mg/kg, ip) for 5 d. Seven days after the last MPTP injection, behavioral testings were performed. The levels of tyrosine hydroxylase (TH) and macrophage antigen (MAC)-1 were determined with immunohistochemistry. The expression of iNOS and COX-2 was measured using RT PCR. Results: In MPP + -treated rat mesencephalic cultures, 6-shogaol significantly increased the number of TH-IR neurons and suppressed TNF-α and NO levels. In C57/BL mice, treatment with 6-shogaol reversed MPTP-induced changes in motor coordination and bradykinesia. Furthermore, 6-shogaol reversed MPTP-induced reductions in TH-positive cell number in the substantia nigra pars compacta (SNpc) and TH-IR fiber intensity in stratum (ST). Moreover, 6-shogaol significantly inhibited the MPTP-induced microglial activation and increases in the levels of TNF-α, NO, iNOS, and COX-2 in both SNpc and ST. Conclusion: 6-Shogaol exerts neuroprotective effects on DA neurons in in vitro and in vivo PD models.

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Section: Discussionmentioning

confidence: 99%

6-Shogaol, an active compound of ginger, protects dopaminergic neurons in Parkinson's disease models via anti-neuroinflammation

Park

Kim

et al. 2013

Acta Pharmacol Sin

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“…Surprisingly, in an ante-mortem study, no change was observed in the NE levels in the frontal cortex, but significant decrease was observed in the temporal cortex [180]. Loss of norepinergic neurons of the LC and subsequent loss of norepinephrine have a pro-inflammatory effect in animal models [181]. Moreover, observation suggests, stimulation of the microglia with norepinephrine leads to enhanced phagocytosis of amyloid-β (Aβ) [181].…”

Section: Review Amarendranath Choudhurymentioning

confidence: 99%

“…Loss of norepinergic neurons of the LC and subsequent loss of norepinephrine have a pro-inflammatory effect in animal models [181]. Moreover, observation suggests, stimulation of the microglia with norepinephrine leads to enhanced phagocytosis of amyloid-β (Aβ) [181]. Therefore, alterations of the norepinergic system contribute partially to the neuroinflammation associated with AD and the subsequent consequences [181].…”

Section: Review Amarendranath Choudhurymentioning

confidence: 99%

“…Moreover, observation suggests, stimulation of the microglia with norepinephrine leads to enhanced phagocytosis of amyloid-β (Aβ) [181]. Therefore, alterations of the norepinergic system contribute partially to the neuroinflammation associated with AD and the subsequent consequences [181]. The NE receptors and transporters may be associated with AD related behaviour.…”

Section: Review Amarendranath Choudhurymentioning

confidence: 99%

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Neurochemicals, Behaviours and Psychiatric Perspectives of Neurological Diseases

Choudhury¹,

Sahu²,

Ramanujam³

et al. 2018

Neuropsychiatry

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Structural changes in different regions of the brain have become clinically relevant and regarded as the signature phenomenon for neurological diseases. Morphological changes in brain are also associated with neuronal and neurochemical alterations. Studies have showed that minute changes in neurochemical levels may have marked impact on the psychobehaviour of the subject. Several neurological disease profiles have been reported with such specific psychobehavioural expression. However, application of behavioural abnormalities as possible disease progress markers has not been considered and emphasised much. Reports suggested that-the subjects, who have already entered into the terminal stage of the disease, used to show cardinal behavioural signs for a specific disease profile. However, psychological expressions are comparatively early expressive. As most of the neurodegenerative disorders are unidirectional and progressive by nature, therapeutic intervention at the right time is essential for attaining the desired outcome. Moreover, early diagnosis can aid in managing the disease progression also. Psychobehavioural analysis could meet the expected outcome of disease diagnosis if implemented properly and timely. In the present review, we have amalgamated the reported behavioural anomalies with the supportive background from neurochemical basis. Further, we have concluded that behaviour centric studies could be a potential diagnostic tool for the early diagnosis of major neurological diseases such as Alzheimer disease, Parkinson's disease, Amyotrophic lateral sclerosis (ALS), Bipolar disorder, Schizophrenia, Impulse control disorder (ICD) and Obsessive-compulsive disorder (OCD).

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“…In contrast to other tissues, the blood-brain barrier (BBB) largely avoids the infiltration of T cells from capillaries. Moreover, astrocytes and neurons are able to suppress T cell activation and even induce apoptosis in T cells [43]. The reason for this Bimmune privilege^in the brain is attributed to its sensitivity and restricted regenerative capacity compared to other tissues.…”

Section: Introductionmentioning

confidence: 99%

Supportive or detrimental roles of P2Y receptors in brain pathology?—The two faces of P2Y receptors in stroke and neurodegeneration detected in neural cell and in animal model studies

Förster

Reiser

2015

Purinergic Signalling

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This review describing the role of P2Y receptors in neuropathological conditions focuses on obvious differences between results demonstrating either a role in neuroprotection or in neurodegeneration, depending on in vitro and in vivo models. Such critical juxtaposition puts special emphasis on discussions of beneficial and detrimental effects of P2Y receptor agonists and antagonists in these models. The mechanisms reported to underlie the protection in vitro include increased expression of oxidoreductase genes, like carbonyl reductase and thioredoxin reductase; increased expression of inhibitor of apoptosis protein-2; extracellular signal-regulated kinase-and Akt-mediated antiapoptotic signaling; increased expression of Bcl-2 proteins, neurotrophins, neuropeptides, and growth factors; decreased Bax expression; non-amyloidogenic APP shedding; and increased neurite outgrowth in neuronal cells. Animal studies investigating the influence of P2Y receptors in middle cerebral artery occlusion (MCAO) models for stroke prove beneficial effects of P2Y receptor antagonists. In MCAO mice and rats, the application of broad-range P2 receptor antagonists decreased the infarct volume and improved neurological outcome. Moreover, antagonists of the P2Y 1 receptor, one of the most abundant P2Y receptor subtypes in brain tissue, decreased neuronal loss and improved spatial memory in rats after traumatic brain injury (TBI). Currently available data show a discrepancy between in vitro and in vivo models concerning the benefits of P2Y receptor activation in pathological conditions. In vitro models demonstrate protection by P2Y receptor agonists, but in vivo P2Y receptor activation deteriorates the outcome after MCAO and controlled cortical impact brain injury, a TBI model. To broaden the scope of the review, we additionally discuss publications that demonstrate detrimental effects of P2Y receptor agonists in vitro and publications showing protective effects of agonists in vivo. All these studies help to better understand the significant role of P2Y receptors especially in stroke models and to develop pharmacological strategies for the treatment of stroke.

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Inflammation in neurodegenerative diseases

Cited by 1,174 publications

References 115 publications

6-Shogaol, an active compound of ginger, protects dopaminergic neurons in Parkinson's disease models via anti-neuroinflammation

6-Shogaol, an active compound of ginger, protects dopaminergic neurons in Parkinson's disease models via anti-neuroinflammation

Neurochemicals, Behaviours and Psychiatric Perspectives of Neurological Diseases

Supportive or detrimental roles of P2Y receptors in brain pathology?—The two faces of P2Y receptors in stroke and neurodegeneration detected in neural cell and in animal model studies

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