Neuroinflammation and Alteration of the Blood-Brain Barrier in Alzheimer´s Disease

Soto-Rojas, Luis O.; Cruz-López, Fidel de la; Torres, Miguel AngelOntiveros; Viramontes-Pintos, Amparo; CarmenCárdenas-Aguayo, María del; Meraz-Ríos, Marco Antonio; Salinas-Lara, Citlaltépetl; Florán, Benjamí­n; Luna-Muñoz, José

doi:10.5772/60024

Cited by 8 publications

(9 citation statements)

References 120 publications

(146 reference statements)

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“…Since AD atrophy results from the degeneration of synapses [45] , in our final experiment, the results indicated that Aβ 1–42 caused a significant increase (6 fold) in the uptake of the fluorescent dye FM1–43 and therefore induced an increase in synaptic activity. When TQ was co-administrated there was a decrease in the synaptic activity by 2.6-fold compared to Aβ 1–42 treated samples.…”

Section: Discussionmentioning

confidence: 68%

Neuroprotective efficacy of thymoquinone against amyloid beta-induced neurotoxicity in human induced pluripotent stem cell-derived cholinergic neurons

Alhibshi

Odawara

Suzuki

2019

Biochemistry and Biophysics Reports

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The natural antioxidant Thymoquinone (TQ) is the most abundant ingredient in the curative plant Nigella sativa seed's oil. An extensive number of studies have revealed that TQ is the most active and most responsible component for the plant's pharmacological properties. It has been documented in several studies that TQ has a wide range of protective activities and many neuropharmacological attributes. Amyloid beta (Aβ) is the major role player peptide in the progression of Alzheimer's disease (AD). Our current study has been implemented to explore the protective possibilities of TQ on Aβ1–42 -induced neurotoxicity. To test TQ's effect we used cultured human induced pluripotent stem cell (hiPSC)-derived cholinergic neurons. The obtained results showed that Aβ1–42 caused cell death and apoptosis, which was efficiently attenuated by the co-treatment of TQ. Moreover, TQ restored the decrease in the intracellular antioxidant enzyme glutathione levels and inhibited the generation of reactive oxygen species induced by Aβ1–42. Furthermore, using the fluorescent dye FM1–43 we demonstrated that TQ was able to reduce synaptic toxicity caused by Aβ1–42. Thus, the findings of our study suggest that TQ holds a neuroprotective potential and could be a promising therapeutic agent to reduce the risk of developing AD and other disorders of the central nervous system.

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Section: Discussionmentioning

confidence: 68%

Neuroprotective efficacy of thymoquinone against amyloid beta-induced neurotoxicity in human induced pluripotent stem cell-derived cholinergic neurons

Alhibshi

Odawara

Suzuki

2019

Biochemistry and Biophysics Reports

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“…Caffeine increased expression of antiapoptotic protein Bcl-2 and reduced expression of proapoptotic protein BAX in the AlCl 3 -induced and Aβ 25-35 -induced neurotoxicity in human neuroblastoma SH-SY5Y cells. Caffeine inhibited also the increase of AD-related proteins (APP and BACE-1) expression in cells exposed to both AlCl 3 and Aβ [25][26][27][28][29][30][31][32][33][34][35] . The effects of caffeine were similar to those induced by selective A 1 R or A 2A R antagonists, indicating the role of blockade of both A 1 R and A 2A R. Caffeine reduced also oxidative stress (reducing NF-κB activity, reducing ROS production, increasing superoxide dismutase (SOD) activity and decreasing MDA concentration) induced by AlCl 3 and Aβ 25-35 .…”

Section: In Vitro Studiesmentioning

confidence: 90%

“…Brain atrophy observed in AD results from the synaptic degeneration and neuronal cell death. Dysfunctions occur mainly in the brain regions that play a major role in memory and spatial orientation, i.e., in the hippocampus, striatum, cerebral cortex, thalamus and amygdala [ 32 , 33 ]. Besides cognitive dysfunctions, the majority of patients with AD suffer from behavioral and psychological symptoms of dementia (BPSD).…”

Section: Alzheimer’s Disease (Ad)mentioning

confidence: 99%

Potential of Caffeine in Alzheimer’s Disease—A Review of Experimental Studies

et al. 2021

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Alzheimer’s disease (AD) is the most common type of dementia leading to progressive memory loss and cognitive impairment. Considering that pharmacological treatment options for AD are few and not satisfactory, increasing attention is being paid to dietary components that may affect the development of the disease. Such a dietary component may be caffeine contained in coffee, tea or energy drinks. Although epidemiological data suggest that caffeine intake may counteract the development of cognitive impairment, results of those studies are not conclusive. The aim of the present study is to review the existing experimental studies on the efficacy of caffeine against AD and AD-related cognitive impairment, focusing on the proposed protective mechanisms of action. In conclusion, the reports of studies on experimental AD models generally supported the notion that caffeine may exert some beneficial effects in AD. However, further studies are necessary to elucidate the role of caffeine in the effects of its sources on cognition and possibly AD risk.

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“…AD is characterized by a progressive deterioration of cognitive functions that can be linked to a significant reduction of the volume of the brain in AD patients as compared to healthy patients [10] . The atrophy results from the degeneration of synapses and the death of neurons, in particular in hippocampus [11] , the brain region playing a role in memory and spatial orientation. The age is the highest risk factor for AD, the risk of developing the disease reaching 50% for individuals beyond age 85 [9] .…”

Section: Linking Oxidative Stress and Admentioning

confidence: 99%

Oxidative stress and the amyloid beta peptide in Alzheimer’s disease

et al. 2018

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Oxidative stress is known to play an important role in the pathogenesis of a number of diseases. In particular, it is linked to the etiology of Alzheimer’s disease (AD), an age-related neurodegenerative disease and the most common cause of dementia in the elderly. Histopathological hallmarks of AD are intracellular neurofibrillary tangles and extracellular formation of senile plaques composed of the amyloid-beta peptide (Aβ) in aggregated form along with metal-ions such as copper, iron or zinc. Redox active metal ions, as for example copper, can catalyze the production of Reactive Oxygen Species (ROS) when bound to the amyloid-β (Aβ). The ROS thus produced, in particular the hydroxyl radical which is the most reactive one, may contribute to oxidative damage on both the Aβ peptide itself and on surrounding molecule (proteins, lipids, …). This review highlights the existing link between oxidative stress and AD, and the consequences towards the Aβ peptide and surrounding molecules in terms of oxidative damage. In addition, the implication of metal ions in AD, their interaction with the Aβ peptide and redox properties leading to ROS production are discussed, along with both in vitro and in vivo oxidation of the Aβ peptide, at the molecular level.

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Neuroinflammation and Alteration of the Blood-Brain Barrier in Alzheimer´s Disease

Cited by 8 publications

References 120 publications

Neuroprotective efficacy of thymoquinone against amyloid beta-induced neurotoxicity in human induced pluripotent stem cell-derived cholinergic neurons

Neuroprotective efficacy of thymoquinone against amyloid beta-induced neurotoxicity in human induced pluripotent stem cell-derived cholinergic neurons

Potential of Caffeine in Alzheimer’s Disease—A Review of Experimental Studies

Oxidative stress and the amyloid beta peptide in Alzheimer’s disease

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