Amyloid beta (A beta) peptide aggregating to form a neurotoxic plaque, leading to cognitive deficits, is believed to be one of the plausible mechanisms for Alzheimer's disease (AD). Inhibiting A beta aggregation is supposed to offer a neuroprotective effect to ameliorate AD. A previous report has shown that SLM, a carbazole-based fluorophore, binds to A beta to inhibit the aggregation. However, it is not entirely clear whether the inhibition of A beta aggregation alone would lead to the anticipated neuroprotective effects. In the current study, we intended to examine the protective action of SLM against A beta-induced neurotoxicity in vitro and to evaluate if SLM can decrease the cognitive and behavioral deficits observed in triple transgenic AD mouse model (3xTg-AD). In the in vitro study, neurotoxicity induced by A beta 42 in human neuroblastoma (SH-SY5Y) cells was found to be reduced through the treatment with SLM. In the in vivo study, following one month SLM intraperitoneal injection (1, 2, and 4 mg/kg), 3xTg-AD mice were tested on Morris water maze (MWM) and Y-maze for their cognitive ability and sacrificed for biochemical estimations. Results show that SLM treatment improved the learning and memory ability in 3xTg-AD mice in MWM and Y-maze tasks. SLM also mitigated the amyloid burden by decreasing brain A beta 40 and A beta 42 levels and reduced tau phosphorylation, glycogen synthase kinase-beta activity, and neuroinflammation. From our observations, SLM shows neuroprotection in SH-SY5Y cells against A beta 42 and also in 3xTg-AD mouse model by mitigating the pathological features and behavioral impairments.