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Table 4 Neurobiological effects produced by myricetin

From: Myricetin bioactive effects: moving from preclinical evidence to potential clinical applications

Model Results Ref.
Anxiety
 In vitro and in vivo Dose-dependent reduction in lithium-induced head twitches and anxiolytic activity by altering 5-hydroxytryptamine transmission. [80]
Alzheimer disease
 In vitro Pro-oxidant agent and reduced the formation of ordered amyloid beta (Aβ)42 aggregation. [81]
 In silico Destabilizes the β-sheet ordered amyloid oligomers formed by the undecapeptide Aβ (25–35) model. [82]
 In vitro Marked modulation of metal-induced Aβ aggregation, more than metal-free Aβ aggregation. Increase cell survival rate of Aβ (with metal ions). [83]
 In vitro Increases α-secretase (ADAM10) enzyme activity and decreases of β-secretase (BACE-1). It also exerts neuroprotective activity against Aβ (1–42) with multifunctional role in counteracting AD progress. [84]
 In vitro Dose-dependent inhibition of α-synuclein fibrils formation and destabilization (EC50 = 0.21–1.8 μM). [85]
 In vitro Dose-dependent inhibition of Aβ fibrils formation from fresh Aβ (1–40) and Aβ (1–42). The EC50 value for formation, extension and destabilization Aβ fibrils ranges from 0.13–1.8 μM. [86]
 In vivo Increases the number of hippocampal CA3 pyramidal neurons and survival in a rat model (10 mg/kg). Improved learning and memory in a rat model with AD. [87]
CNS
 In vitro Reduces the aggregation of different abnormal proteins and eliminates various toxic proteins related to neurodegenerative diseases. Improves physiological functions of Hsp70 molecular chaperone and reduces mis-folded proteins. [88]
 In vitro and in vivo Increases GABA receptor activity via calcium channel/ CaMK-II dependent mechanism, which is distinctively different from that of most existing benzodiazepine binding site agonists of GABA receptor. [89]
 In vivo Increases mRNA for brain-derived neurotrophic factor (BDNF) in the hippocampus of male C57BL/6 mice at 10 and 20 mg/kg (7 days). [90]
 In vivo Increases BDNF concentrations in the hippocampus of male C57BL/6 mice at 50 mg/kg (21 days). [91]
 In vivo Enhances expression and activity of ERK1/2-CREB pathway and Na+, K+-ATPase while reduces oxidative stress level in hippocampus. Improves learning and memory when compared with D-galactose. [92]
Epilepsy
 In vivo Reduces seizure severity and mortality rates in mouse models and signaling pathways (BDNF-TrkB) and regulates GAD65/GABA with MMP-9 expression. [93]
Huntington disease
 In vivo Interacts with RNA, especially CAG motif, and decreases the huntingtin protein translation and sequestration. Reduces cytotoxicity in HD and other polyQ disease models. [94]
Parkinson disease
 In vitro Suppresses intracellular ROS production, re-establishes mitochondrial trans-membrane potential, and inhibits MKK4 and JNK activation. [95]
 In vitro and in vivo Inhibits activation of microglia (neuroinflammation), expression of pro-inflammatory mediators and reduces the number of dopaminergic neurons. [96]
 In vivo Dose-dependent delay in climbing ability loss, but increases the life span of flies expressing human α-synuclein in brain. [97]
 In vivo Prevents the loss of dopaminergic neurons and dopamine content in brain of Parkinson flies. [98]
 In vivo Dose-dependent inhibitory activity on α-synuclein aggregation. [99]
 In vivo Diminishes dopamine neuron degeneration, which is induced by 6-hydroxydopamine and 1-methyl-4-phenyl-pyridinium in substantia nigra-striatum. [100]
  1. Aβ amyloid beta, CNS central nervous system, BDNF brain-derived neurotrophic factor