Our previous investigation showed that anchovy protein hydrolysate (APH) could attenuate scopolamine-induced memory deficits in mice by regulating acetylcholinesterase (AChE) activity.
<b>Results:</b> The mice subjected to CD showed weight gain, body fat accumulation, increased glucose, cholesterol, and triglycerides, associated to recognition memory deficits and increased reactive species (RS) levels and acetylcholinesterase (AChE) activity in the hippocampus.
Thus, the aim of this study was to determine the possible preventive effect of guarana powder (Paullinia cupana) on memory impairment and acetylcholinesterase (AChE) activity in the brain structures of rats with Poloxamer-407-induced hyperlipidemia.
Oral administration of lutein (50 mg/kg during 14 days) attenuated memory deficit and the increase of acetylcholinesterase activity induced by ethanol.
In conclusion, N-NS was able to reverse memory impairment and to prevent increased ROS and TBARS levels due to amelioration of Na<sup>+</sup>, K<sup>+</sup>-ATPase and AChE activities and to activation of the antioxidant enzymes, respectively.
Untreated diabetic mice (the group C) showed memory deficit, increased levels of thiobarbituric acid reactive species (TBARS) and protein carbonylation (PC), and decreased (p < 0.05) catalase (CAT), superoxide dismutase (SOD), and the Na<sup>+</sup>, K<sup>+</sup>-ATPase activities, while acetylcholinesterase (AChE) activity showed a significant increase (p < 0.05) compared to non-diabetic mice (the group A).
Systemic administration of SCOP for seven days caused memory impairment which manifested as decreased time spent in platform quadrant in Morris water maze test, decreased retention latencies in passive avoidance test, and increased acetylcholinesterase (AChE) activity, Aβ, and free iron deposition.
Results demonstrated that: (a) a moderate treadmill running exercise prevented spatial learning and memory deficits in aged rats; (b) training in the Water maze increased both Na<sup>+</sup>, K<sup>+</sup>-ATPase and AChE activities in the hippocampus of mature and aged rats; (c) aged exercised rats displayed an even further increase of Na<sup>+</sup>, K<sup>+</sup>-ATPase activity in the hippocampus, (d) enzyme activity correlated with memory performance in aged rats.
In conclusion, the present study showed that treatment with ANT attenuated memory deficits, protected against oxidative damage in the brain, and restored AChE and ion pump activity in an STZ-induced SDAT in rats.
The step-through passive avoidance test, Morris water maze test, acetylcholinesterase (AChE) activity, and expression of cAMP response element-binding protein (CREB) and brain-derived neurotropic factor (BDNF) were employed to determine the effects of FCL on scopolamine-induced memory deficit in mice.
These findings provide one of the first examples of LTD gating under the control of a G protein-coupled receptor that might lead to imbalanced synaptic plasticity and memory impairment following a nonphysiological elevation of extracellular serotonin.
While there are multiple changes in the hippocampal proteome in the irradiated rats that have impaired spatial memory performance, with 203 proteins being detected (or upregulated) only in these rats, it would appear that spatial memory impairment may also arise from an inability of these rats to express "good spatial memory" (GSM) proteins, many of which play an important role in neuronal homeostasis and function, axonogenesis, presynaptic membrane organization and G-protein coupled receptor (GCPR) signaling.
TTBK1-Tg mice show significant age-dependent memory impairment as determined by radial arm water maze test, which is associated with enhancement of tau and neurofilament phosphorylation, increased levels of p25 and p35, both activators of cyclin-dependent protein kinase 5 (CDK5), enhanced calpain I activity, and reduced levels of hippocampal NMDA receptor types 2B (NR2B) and D. Enhanced CDK5/p35 complex formation is strongly correlated with dissociation of F-actin from p35, suggesting the inhibitory mechanism of CDK5/p35 complex formation by F-actin.
Hence, this study sought to evaluate the effect of curcumin on cerebral cortex acetylcholinesterase (AChE) and adenosine deaminase (ADA) activities in cadmium (Cd)-induced memory impairment in rats.
Furthermore, PACAP administration counteracted R6/1 mice memory deficits as analyzed by the novel object recognition test and the T-maze spontaneous alternation task.