Abstract
Cognitive impairment is associated with brain aging or age-dependent neurodegenerative disorders. However, experimental evidence for type 2 diabetes mellitus (DM II)-induced aging process, decline in learning and memory and the underlying mechanisms are not known. Present study was aimed to understand the underpinning molecular and neurobiological mechanisms for above. Also, the study includes whether Bacopa monnieri extract (CDRI-08), a widely acclaimed nootropic drug, possesses neuroprotective role in DM II-induced brain aging and in learning and memory impairments. To understand above, we developed the DM II mice model by i.p. injection of a selected dose of streptozotocin as mentioned in methodology section and thereafter analyzed the level of neuronal lipofuscin, alterations in working and reference memory, AChE activity and dendritic spine density in pre-frontal cortex as well as in hippocampus. Our data revealed a significant increase in the accumulation of lipofuscin and impairments in working and reference memory in streptozotocin-induced DM II mice compared to normal control. It was correlated with increased AChE activity and decreased neuronal spine density in pre-frontal cortex and hippocampus. Oral administration of a selected dose of CDRI-08 to DM II mice significantly reversed the accumulation of lipofuscin, recovered memory loss, decreased the AChE activity and enhanced dendritic spine density towards their values in normal control mice. Current study clearly demonstrates that DM II induces brain aging and CDRI-08 has neuroprotective role in the recovery of DM II-induced aging and cognitive impairments.
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