Implicating the role of lycopene in restoration of mitochondrial enzymes and BDNF levels in β-amyloid induced Alzheimer׳s disease

Prakash, Atish; Kumar, Anil

doi:10.1016/j.ejphar.2014.07.036

Cited by 109 publications

(70 citation statements)

References 51 publications

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“…We observed a marked reduction of brain nitrite levels with lycopene. Very recently, Prakash and Kumar [61,62] also reported that lycopene protects colchicine and Aβ-induced memory impairment in rats by down-regulating NO pathway and Brain-derived neurotrophic factor (BDNF) levels, respectively. In concurrence with these reports, we also observed a marked decrease in brain nitrite levels with lycopene.…”

Section: Discussionmentioning

confidence: 97%

Lycopene abrogates Aβ(1–42)-mediated neuroinflammatory cascade in an experimental model of Alzheimer’s disease

Sachdeva

Chopra

2015

The Journal of Nutritional Biochemistry

163

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Section: Discussionmentioning

confidence: 97%

Lycopene abrogates Aβ(1–42)-mediated neuroinflammatory cascade in an experimental model of Alzheimer’s disease

Sachdeva

Chopra

2015

The Journal of Nutritional Biochemistry

163

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“…Moreover, it also ameliorates the mitochondrial reduction capacity against Aβ AD [130] Lycopene Involves in attenuation of mitochondrial-oxidative damage, memory retention, reduced neuro-inflammation and restoration of BDNF level in Aβ 1-42 treated rats AD [131] Geniposide Exerts protective effects on mitochondrial dysfunction in APP/PS1 mice through increasing the mitochondrial membrane potential, suppressing the mitochondrial oxidative damage and activity of cytochrome c oxidase AD [132] Resveratrol (RSV) Reduces the Aβ burden and contributing to the modulation of autophagy and an increase of mitochondrial biogenesis in mouse brain mediated through increased activation of Sirtuin 1 (Sirt1) and AMP-activated protein kinase (AMPK) pathways. It also protects against diet-induced obesity, improves insulin resistance, induces genes for oxidative phosphorylation, and activates PGC-1α AD, ALS and MetS [133,134] Thiazolidinediones Activates PPAR-γ to reduce insulin resistance (IR) in T2D AD and T2D [133] Dimebon…”

Section: Methazolamide (Mtz)mentioning

confidence: 98%

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Mounting evidence suggests a link between metabolic syndrome (MetS) such as diabetes, obesity, non-alcoholic fatty liver disease in the progression of Alzheimer's disease (AD), Parkinson's disease (PD) and other neurodegenerative diseases (NDDs). For instance, accumulated Aβ oligomer is enhancing neuronal Ca release and neural NO where increased NO level in the brain through post translational modification is modulating the level of insulin production. It has been further confirmed that irrespective of origin; brain insulin resistance triggers a cascade of the neurodegeneration phenomenon which can be aggravated by free reactive oxygen species burden, ER stress, metabolic dysfunction, neuorinflammation, reduced cell survival and altered lipid metabolism. Moreover, several studies confirmed that MetS and diabetic sharing common mechanisms in the progression of AD and NDDs where mitochondrial dynamics playing a critical role. Any mutation in mitochondrial DNA, exposure of environmental toxin, high-calorie intake, homeostasis imbalance, glucolipotoxicity is causative factors for mitochondrial dysfunction. These cumulative pleiotropic burdens in mitochondria leads to insulin resistance, increased ROS production; enhanced stress-related enzymes that is directly linked MetS and diabetes in neurodegeneration. Since, the linkup mechanism between mitochondrial dysfunction and disease phenomenon of both MetS and NDDs is quite intriguing, therefore, it is pertinent for the researchers to identify and implement the therapeutic interventions for targeting MetS and NDDs. Herein, we elucidated the pertinent role of MetS induced mitochondrial dysfunction in neurons and their consequences in NDDs. Further, therapeutic potential of well-known biomolecules and chaperones to target altered mitochondria has been comprehensively documented. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.

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“…Since lycopene has a high liposolubility, it can cross the blood-brain barrier (16). It has also been demonstrated that lycopene is beneficial for certain neurological disorders, including Alzheimer's disease (17,18). Therefore, lycopene is potentially beneficial in other brain diseases and the present study set out to investigate this.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effects of lycopene pretreatment on transient global cerebral ischemia-reperfusion in rats: The role of the Nrf2/HO-1 signaling pathway

Lei

Zhang

et al. 2015

Molecular Medicine Reports

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Abstract. The present study aimed to investigate the neuroprotective effect of lycopene in a mouse model of bilateral common carotid artery occlusion (BCCAO) and the role of the Nrf2/HO-1 signaling pathway. A total of 60 male C57BL/6 mice, aged 12 weeks and weighing 20-24 g, were used in the present study. The mice were randomly assigned to three groups: Control, BCCAO and BCCAO + lycopene. The neurological score was assessed 24, 48 or 72 h following BCCAO. Hematoxylin and eosin staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) were performed to detect neuronal death and survival. The production of glutathione (GSH) and reactive oxygen species were detected to investigate the oxidative stress. The expression levels of nuclear factor erythroid 2-related factor (Nrf2) and Heme oxygenase-1 (HO-1) were determined by western blotting. Lycopene significantly improved the neurological score in the BCCAO mice. It attenuated neuronal apoptosis, as indicated by TUNEL staining, and attenuated the oxidative stress induced by global ischemia. Lycopene increased the expression levels of Nrf2 and HO-1, indicating that the Nrf2/HO-1 signaling pathway may be involved in the neuroprotective effect of lycopene. The present study revealed that lycopene protects the brain from global ischemic injury, which is associated with its antiapoptotic effect and the activation of the Nrf2/HO-1 signaling pathway.

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Implicating the role of lycopene in restoration of mitochondrial enzymes and BDNF levels in β-amyloid induced Alzheimer׳s disease

Cited by 109 publications

References 51 publications

Lycopene abrogates Aβ(1–42)-mediated neuroinflammatory cascade in an experimental model of Alzheimer’s disease

Lycopene abrogates Aβ(1–42)-mediated neuroinflammatory cascade in an experimental model of Alzheimer’s disease

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Neuroprotective effects of lycopene pretreatment on transient global cerebral ischemia-reperfusion in rats: The role of the Nrf2/HO-1 signaling pathway

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