Because mitochondrial dysfunction and cognitive impairment also occur together in many neurodegenerative conditions there may be broad therapeutic potential of NRF2 activating agents.
Chotosan ameliorates cognitive impairment and hippocampus neuronal loss in experimental vascular dementia via activating the Nrf2-mediated antioxidant pathway.
Thus, we predict that HBA might prevent Aβ42 oligomer-induced synapse and cognitive impairments through multiple targets including increasing Nrf2, increasing neurotrophic factors and decreasing inflammatory factors.
Based on the role of inflammation and cognitive impairment in the prodromal state, early intervention using anti-inflammatory compounds (i.e., D-serine, sodium benzoate, TrkB agonist, Nrf2 agonist, soluble epoxide hydrolase inhibitor) may reduce the risk of subsequent transition to schizophrenia.
Activation of Nrf2/ARE pathway alleviates the cognitive deficits in PS1V97L-Tg mouse model of Alzheimer's disease through modulation of oxidative stress.
Further studies showed that DOPS could attenuate oxidative stress and reduce neuro-inflammation via up-regulating expressions of Nrf2/HO-1 pathway and inhibiting activation of astrocytes and microglia in ovariectomy- and d-galactose-induced cognitive decline.
This study aims to test whether sulforaphane (Sfn), a natural activator of nuclear factor erythroid 2-related factor 2 (Nrf2), reduces the chronic ischemic injury and cognitive dysfunction after VCI.
Moreover, classic signs of cognitive impairment and deficits in spatial learning and memory were observed in the neurobehavioral tests.<i>E. officinalis</i> tannins exhibited good affinity to Nrf2 receptors in <i>in silico</i> studies, significantly reversed the changes in the aforementioned biomarkers of oxidative stress which were altered in the model group, as well as improved the performance of rats in Morris water maze task.
Thus, these data suggest that alleviation of the sustained mitochondrial dysfunction and oxidative stress through co-modulation of NRF2 and PINK1 may be in charge of restoration of the cognitive impairments in a mouse model of high-LET carbon ion irradiation.
Protective Effects of Sulforaphane on Cognitive Impairments and AD-like Lesions in Diabetic Mice are Associated with the Upregulation of Nrf2 Transcription Activity.
This study was aimed at determining effect of troxerutin on the development of cognitive dysfunction and the expression level of Nrf2 in the hippocampus of streptozotocin (STZ) diabetic rats, when used in the early preventive stage.
As the post-injury functional outcome depends on the balance of these opposing molecular pathways, we evaluated the effect of TBI on the motor and cognitive deficits and cortical contusion volume in NOX2 and Nrf2 knockout mice.
In conclusion, the expression of Nrf2-ARE molecules and related antioxidases is significantly decreased in patients with OSAHS and is correlated with neurocognitive dysfunction.
NFE2L2rs6721961 T allele was associated with a reduced risk of PD (OR = 0.70, 95% CI = 0.53, 0.94) and slower cognitive decline (β = 0.095; p = 0.0004).
RESULTS Aging led to a decline in cognitive function compared with SAMR1 mice and the Nrf2-shRNA-lentivirus further exacerbated the cognitive impairment in SAMP8 mice.
Our results provide evidence indicating that JQ1 treatment could modulate Nox4-Nrf2 redox imbalance in the hippocampus and may be a promising agent for diabetes-associated cognitive dysfunction.
We first describe that NRF2-knockout (Nrf2<sup>-/-</sup>) mice exhibit impaired long term potentiation, a function that requires integrity of the SGZ, therefore suggesting a cognitive deficit that might be linked to hippocampal neurogenesis.