ORIGINAL ARTICLE Rhizophora mucronata attenuates beta-amyloid induced cognitive dysfunction, oxidative stress and cholinergic deficit in Alzheimer’s disease animal model Natarajan Suganthy 1 & Dicson Sheeja Malar 1 & Kasi Pandima Devi 1 Received: 28 December 2015 /Accepted: 28 April 2016 # Springer Science+Business Media New York 2016 Abstract Alzheimer’s disease (AD) is a progressive neuro- degenerative disorder, characterized by accumulation and de- position of Aβ peptide in human brain. The present study aimed to determine the protective effect of catechin rich ex- tract of MERM (methanolic extract of Rhizophora mucronata) on Aβ (25–35) induced cognitive impairment and neuronal toxicity in mice. In the present study AD char- acteristics were induced by intracerberoventricular adminis- tration of aggregated Aβ (25–35) in the Swiss albino mice. Learning and memory deficits were assessed using behavioral assays such as Morris water maze, Y-maze and step down avoidance tasks. Oxidative stress mediated impairment were assessed by measuring the activities of enzymatic and non- enzymatic antioxidants, level of apoptotic protein and oxida- tive markers in the hippocampus and frontal cortex region. Histolopathological analysis of brain was also carried out. Results illustrated that oral treatment of MERM (200 and 400 mg/kg bw) significantly attenuated Aβ (25–35) induced memory impairment as evaluated by behavioral tests. In addi- tion treatment with MERM attenuated the elevation of β- secretase activity accompanying the reduced level of Aβ (25–35) in the cortex and hippocampus of brain. MERM also enhanced the cognitive function by significantly inhibiting AChE, BuChE and MAO-B. Furthermore, MERM attenuated lipid peroxidation, protein oxidation, restored the antioxidant status and inhibited neuronal apoptosis by down-regulating the level of caspase 3 and Bax protein. These data suggest that MERM rich in catechin can act as promising drug for AD treatment because of its antioxidant, anti-apoptotic and reduc- ing Aβ oligomer activities. Keywords Rhizophora mucronata . Aβ (25–35) . Cognitive impairment . Oxidative stress . β-secretase . Apoptosis Introduction Alzheimer’s disease (AD) is an irreversible, progressive and degenerative disorder damaging the higher structures of the brain, characterized by cognitive decline at its onset followed by deficits in multiple cortical functions in later stages (Marchesi 2012). Aβ has been thought to be a critical factor in the pathogenesis of AD. Many studies have found that the accumulation of Aβ in the brain is associated with oxidative stress induced neuronal death and cognitive deficits (Ianiski et al. 2012). Therefore, preventing the neurotoxicity induced by Aβ might be an optimal strategy for treatment of AD. Aβ (25–35) is considered as the shorter toxic fragment exerting neurotoxic effects similar to those produced by Aβ (1–40/42) in mice, such as learning and memory impairment, neuronal apoptosis, cholinergic dysfunction, and oxidative stress, hence Aβ (25–35) administered mice is widely used as AD model for study of the neurotoxic properties of Aβ and drug screen- ing (Villard et al. 2008; Liu et al. 2009). Current clinical treat- ments of AD patients use acetylcholinesterase inhibitors (AChEIs) and antagonists of N-methyl-D-aspartate receptors (NMDA) to slow down the progress of neuronal deterioration in AD (Mehta et al. 2012). The lack of drugs in treatment and prevention of AD combining high efficacy and low side ef- fects has stimulated the search for novel agents that might represent a new therapy. Preliminary studies on neuroprotec- tive effect of catechin rich extract of MERM showed antiox- idant and cholinesterase inhibitory activity in cell free in vitro * Kasi Pandima Devi devikasi@yahoo.com 1 Department of Biotechnology, Alagappa University, Karaikudi, Tamil Nadu 630 003, India Metab Brain Dis DOI 10.1007/s11011-016-9831-0