Abstract
Memory is an essential aspect of human cognition. A decrease in this aspect is well associated with Alzheimer’s disease (AD). The development of a novel cognitive enhancer (CE) may help overcome AD-related problems. In this study, we evaluated the CE effect of Caesalpinia sappan L. (CS) in memory deficit mice. Administration of its ethanolic extract (250 and 500 mg/kg body weight (BW)) and brazilin (5 and 10 mg/kg BW) ameliorated the scopolamine-amnesic effect, as evidenced by significant decreases (p < 0.01, p < 0.05) in the escape latency time and increases (p < 0.01) in the percentage of time spent in the target quadrant of the Morris water maze test. We also examined the cyclic adenosine monophosphate (cAMP) level, protein kinase A (PKA) activity, and protein expression levels of phosphorylated cAMP response element binding (pCREB) and brain-derived neurotrophic factor (BDNF) in hippocampal tissues to elucidate the underlying molecular mechanism. Results showed that CS wood ethanolic extract and brazilin not only significantly increase (p < 0.01, p < 0.05) cAMP levels and PKA activity but also significantly enhance (p < 0.01, p < 0.05) the expression level of pCREB and BDNF in the hippocampus. These findings indicate that CS activates the cAMP/PKA/CREB/BDNF pathway. Taken together, our results demonstrate that CS is a promising herb that could be developed as a CE agent.
Highlights
Reductions in cyclic nucleotides (e.g., cyclic adenosine monophosphate and/or cGMP) and neurotrophic proteins (e.g., brainderived neurotrophic factor (BDNF)) in the brain have been observed to be positively correlated with Alzheimer’s disease (AD) progression
The extract was extract manifested by a presence of brazilin in the manifested by ato single single strong peak with a The maximum retention factor (Rf)extract of 0.69was
CEsknown are that are applied for amnesia amelioration in AD;inthese compounds exert drugs”
Summary
Dementia is a neurological syndrome characterized by a progressive decline in cognitive function. The most common type of dementia is Alzheimer’s disease (AD) [1,2,3]. Abnormal proteins in the brain, amyloid plaques, and neurofibrillary tangles are common features of the disease and affect central functions, such as memory [4,5,6]. Memory is one of prominent aspects of assessing cognition in AD. Impairments in memory are clinically observed in patients with AD and are linked to dysfunctions of the hippocampus and the prefrontal lobe region [7,8]. Reductions in cyclic nucleotides (e.g., cyclic adenosine monophosphate (cAMP) and/or cGMP) and neurotrophic proteins (e.g., brainderived neurotrophic factor (BDNF)) in the brain have been observed to be positively correlated with AD progression
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