A review of behavioral methods for the evaluation of cognitive performance in animal models: Current techniques and links to human cognition.

INTRODUCTION: Memory is defined as the ability to store, maintain and retrieve information. Learning is the acquisition of information that changes behavior and memory. Stress, dementia, head trauma, amnesia, Alzheimer's, Huntington, Parkinson's, Wernicke-Korsakoff syndrome (WKS) may be mentioned among the diseases in which memory and learning are affected. The task of understanding deficits in memory and learning in humans is daunting due to the complexity of neural and cognitive mechanisms in the nervous system. This job is made more difficult for clinicians and researchers by the fact that many techniques used to research memory are not ethically acceptable or technically feasible for use in humans. Thus, animal models have been necessary alternative for studying normal and disordered learning and memory. This review attempts to bridge these domains to allow biomedical researchers to have a firm grasp of "memory" and "learning" as constructs in humans whereby they may then select the proper animal cognitive test. RESULTS AND CONCLUSION: Various tests (open field habituation test, Y-maze test, passive avoidance test, step-down inhibitory avoidance test, active avoidance test, 8-arms radial maze test, Morris water maze test, radial arm water maze, novel object recognition test and gait function test) have been designed to evaluate different kinds of memory. Each of these tests has their strengths and limits. Abnormal results obtained using these tasks in non-human animals indicate malfunctions in memory which may be due to several physiological and psychological diseases of nervous system. Further studies by using the discussed tests can be very beneficial for achieving a therapeutic answer to these diseases.

Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways.

Neurodegeneration is a gradual mechanism of neuronal loss arising from numerous cellular and molecular events such as mitochondrial dysfunction, oxidative stress, inflammation, and apoptosis, and the consequence of these processes is neuroplasticity impairment, cognitive diseases, mood-related diseases, and normal cellular activity. Over the last year, major advances have been made in the field of the introduction of herbal compounds with neuroprotective efficacy, one of which is curcumin. Curcumin (diferuloylmethane) is the most abundant turmeric component extracted from the Curcuma longa plant rhizomes. Accumulating evidence indicates that curcumin may induce mitochondrial biogenesis and can function as an antioxidant, anti-inflammatory, and anti-apoptotic agent, which may be used effectively to treat chronic neurodegenerative diseases and any situation in which the neurodegeneration process takes place. Curcumin has been shown to play a critical role in activating two essential signaling pathways phosphatidylinositol-3(PI3)/ protein kinase B(Akt)/ glycogen synthase kinase-3 (GSK3) and PI3/Akt/cAMP response element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF) and preventing the incidence of neurodegeneration via these two pathways. Curcumin's protective functions against neural cell degeneration due to mitochondrial dysfunction and consequent events such as oxidative stress, inflammation, and apoptosis in neural cells have been documented and clinical data have increased to suggest that curcumin may be a standard candidate as a neuroprotective agent. Therefore, in this review, we summarized the clinical and experimental studies and interpreted the key contributory mechanisms of neuroprotective properties of curcumin in neurodegenerative diseases and disorders. We also tried to understand the function of PI3/Akt/GSK3 and PI3/Akt/CREB/BDNF signaling pathways in the neuroprotective properties of curcumin and tried to evaluate their association with antioxidant, anti-inflammatory, anti-apoptosis and biogenesis effects of mitochondria.