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Cited by 27 publications
(17 citation statements)
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“…AD is a neurodegenerative disease characterized by progressive dementia, neuroinflammation, intracellular neurofibrillary tangles and accumulation of extracellular plaques. There appear to be four main causes: the hypothesis of abnormal folding and aggregation of amyloid-beta/tau protein, activation of the innate immune system, mitochondrial dysfunction and oxidative stress [9]. In this study, we collected the gene expression profiles and normal control brain tissues of AD in GSE110226 from GEO.…”
Section: Discussionmentioning
confidence: 99%
“…AD is a neurodegenerative disease characterized by progressive dementia, neuroinflammation, intracellular neurofibrillary tangles and accumulation of extracellular plaques. There appear to be four main causes: the hypothesis of abnormal folding and aggregation of amyloid-beta/tau protein, activation of the innate immune system, mitochondrial dysfunction and oxidative stress [9]. In this study, we collected the gene expression profiles and normal control brain tissues of AD in GSE110226 from GEO.…”
Section: Discussionmentioning
confidence: 99%
“…In this heterogeneous group of substances, many subclasses have been identified such as stilbenoids, flavonoids, curcuminoids, phenolate esters, and lignans. These compounds showed an effect against the Aβ peptide and tau pathologies, on the activation of the inflammation response, on the oxidative stress, and also on the mitochondrial dysfunction (Kolaj et al, 2018). Between others, resveratrol , quercetin , wogonin , epigallocatechin-3-gallate ( EGCG ), and curcumin were already tested and showed to promote mitochondrial biogenesis, to impede apoptotic pathways through inhibition of DNA fragmentation, ROS formation, and caspase-3 activation, and to reduce perturbation of mtΔΨ and ATP levels (see also Table 1 for the effects of phenylpropanoids on mitochondria in AD models) (Lagouge et al, 2006; Davis et al, 2009; Im et al, 2012; Valenti et al, 2013; Reddy et al, 2016).…”
Section: Mitochondrial Therapies In Admentioning
confidence: 99%
“…Besides all the compounds listed until now, there are several other molecules which may act at the same time on many pathways linked to mitochondrial dysfunctions (for a general overview see Table 5). For example, phenylpropanoids are natural molecules derived from the amino acid l-phenylalanine; among them, resveratrol, curcumin, and flavonoids (including epigallocatechin-gallate, quercetin and wogonin) can (i) regulate mitochondrial biogenesis, enhancing the expression of several activators (i.e., PGC-1α, SIRT1, Nrf1, Nrf2, and TFAM), (ii) improve mitochondrial bioenergetics, (iii) enhance ATP production, and (iv) counteract apoptotic pathways (as described in Kolaj et al [212]). Furthermore, they are able to prevent oxidative stress (i) quenching free radicals through a direct mechanism [213], (ii) upregulating the expression of antioxidative enzymes via the activation of different signaling pathways (i.e., Nrf2), even increasing GSH production [214,215], and (iii) inhibiting ROS-forming enzymes like XO and NOX [216].…”
Section: Compounds Targeting Multiple Mitochondrial Dysfunctionsmentioning
confidence: 99%