Antroquinonol administration in animal preclinical studies for Alzheimer's disease (AD): A new avenue for modifying progression of AD pathophysiology

Fernández, Francisco Sousa; Aust, Caitlin E.; Lye, Sarah; Griffiths, Lyn R.

doi:10.1016/j.bbih.2022.100435

Cited by 5 publications

(3 citation statements)

References 63 publications

(82 reference statements)

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“…Here, we observed a reduction in the level of Nrf2 and an elevation in the level of NOX4 in astrocytes in the frontal cortex of AD patients, in the cortex of 3×Tg mice, and in mouse astrocytes. This finding is in line with previous reports of Nrf2 reduction in cortical brain tissue from AD patients [24] and in brain tissue from 3×Tg mice [60]. Elevation of the level of NOX4 and its involvement in promoting the ferroptosis of astrocytes has been reported in the postmortem brain from AD and APP/PS1 mice [24].…”

Section: Discussionsupporting

confidence: 92%

NRF2 Deficiency Promotes Ferroptosis of Astrocytes Mediated by Oxidative Stress in Alzheimer’s Disease

Tang,

Chen,

Guo

et al. 2024

Mol Neurobiol

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Oxidative stress is involved in the pathogenesis of Alzheimer's disease (AD), which is linked to reactive oxygen species (ROS), lipid peroxidation, and neurotoxicity. Emerging evidence suggests a role of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), a major source of antioxidant response elements in AD. The molecular mechanism of oxidative stress and ferroptosis in astrocytes in AD is not yet fully understood. Here, we aim to investigate the mechanism by which Nrf2 regulates the ferroptosis of astrocytes in AD. Postmortem frontal cortex tissues from patients with AD and nondemented controls and brain tissue from the 3×Tg AD mouse model and wild-type mice (10 months old) were used. Immunofluorescence staining for Nrf2, the ROS marker NADPH oxidase 4 (NOX4), and GFAP was performed.We further induced Nrf2 deficiency in mouse astrocytes by using RNAi and assessed the changes in ROS, ferroptosis, lipid peroxidation, and mitochondrial dysfunction by using western blotting and immunofluorescence staining. We found decreased expression of Nrf2 and upregulated expression of NOX4 in the frontal cortex from patients with AD and in the cortex of 3×Tg mice compared to control mice. We demonstrated that Nrf2 deficiency led to ferroptosis-dependent oxidative stress-induced ROS with downregulated heme oxygenase-1 and glutathione peroxidase 4 and upregulated cystine glutamate expression. Moreover, Nrf2 deficiency increased lipid peroxidation, DNA oxidation, and mitochondrial fragmentation in mouse astrocytes. In conclusion, these results suggest that Nrf2 promotes ferroptosis of astrocytes involving oxidative stress in AD..

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Section: Discussionsupporting

confidence: 92%

NRF2 Deficiency Promotes Ferroptosis of Astrocytes Mediated by Oxidative Stress in Alzheimer’s Disease

Tang,

Chen,

Guo

et al. 2024

Mol Neurobiol

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“…Frontiers in Pharmacology frontiersin.org stress markers showed a significant decrease (Francesca et al, 2022).…”

Section: Antioxidant Activitiesmentioning

confidence: 97%

“…As the catalytic subunit of deacetylase repressor complexes, the increase of HDAC2 level and activity in AD have been linked to the worsening of neuronal and synaptic function ( Gonzalez-Zuninga et al, 2014 ). Further antroquinonol administration studies showed that anxiety-related behavior and cognitive abilities in 3XTgAD mice could be significantly improved; furthermore, inflammatory markers, AD biomarkers, and oxidative stress markers showed a significant decrease ( Francesca et al, 2022 ). The results are consistent with previously study in the APP transgenic mice, which confirmed the antioxidant capacity of antroquinonol in AD model.…”

Section: Neuroprotection Potential Of Acmentioning

confidence: 99%

Current and further outlook on the protective potential of Antrodia camphorata against neurological disorders

Li,

Wan,

Qiao

et al. 2024

Front. Pharmacol.

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Prevalent neurological disorders such as Alzheimer’s disease, Parkinson’s disease, and stroke are increasingly becoming a global burden as society ages. It is well-known that degeneration and loss of neurons are the fundamental underlying processes, but there are still no effective therapies for these neurological diseases. In recent years, plenty of studies have focused on the pharmacology and feasibility of natural products as new strategies for the development of drugs that target neurological disorders. Antrodia camphorata has become one of the most promising candidates, and the crude extracts and some active metabolites of it have been reported to play various pharmacological activities to alleviate neurological symptoms at cellular and molecular levels. This review highlights the current evidence of Antrodia camphorata against neurological disorders, including safety evaluation, metabolism, blood-brain barrier penetration, neuroprotective activities, and the potential on regulating the gut-microbiome-brain axis. Furthermore, potential strategies to resolve problematic issues identified in previous studies are also discussed. We aim to provide an overview for the ongoing development and utilization of Antrodia camphorata in cerebral neuropathology.

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Brain-targeted Tet-1 peptide-PLGA nanoparticles for berberine delivery against STZ-induced Alzheimer’s disease in a rat model: Alleviation of hippocampal synaptic dysfunction, Tau pathology, and amyloidogenesis

Saleh,

Abd-Elmegied,

Aly Madhy

et al. 2024

International Journal of Pharmaceutics

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Antroquinonol administration in animal preclinical studies for Alzheimer's disease (AD): A new avenue for modifying progression of AD pathophysiology

Cited by 5 publications

References 63 publications

NRF2 Deficiency Promotes Ferroptosis of Astrocytes Mediated by Oxidative Stress in Alzheimer’s Disease

NRF2 Deficiency Promotes Ferroptosis of Astrocytes Mediated by Oxidative Stress in Alzheimer’s Disease

Current and further outlook on the protective potential of Antrodia camphorata against neurological disorders

Brain-targeted Tet-1 peptide-PLGA nanoparticles for berberine delivery against STZ-induced Alzheimer’s disease in a rat model: Alleviation of hippocampal synaptic dysfunction, Tau pathology, and amyloidogenesis

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