Background: Trans-Sinapic Acid is a bioactive compound. Recent studies showed that it
has a significant potential to attenuate various chemically induced Neurodegenerative toxicities.
Aim: The present study investigates the potential of trans-Sinapic Acid as neuromodulator and its effect
on release of Monoamine Oxidase (MAO-A, MAO-B), TNF-α, Acetylcholine esterase Enzyme, in
cognitive dysfunctions associated with experimental dementia.
Experiment: Aluminium chloride was administered at a dose of 175mg/kg, p.o. for a period of 25 days
in rats and then divided into different groups, i.e. Treatment group, negative control and two groups of
trans- Sinapic Acid, (at a dose of 30 and 60mg/kg, p.o.), where these groups treated and observed until
the 35th day of experimental trial. Morris water Maze (MWM) and Photoactometer was used to access
learning, memory and ambulatory movements on 5th, 16th, 26th and 36th day of experiment. Later, the
animals were sacrificed for biochemical and histopahological studies. The oxidative stress was measured
by estimating the levels of Glutathion (GSH), Superoxide dismutase (SOD), Nitrite, Catalase.
Brain acetylcholine esterase (Ache) activity and Monoamine oxidase (MAO-A, MAO-B) were also
estimated. The Brain level of TNF-α was measured as a marker of inflammation.
Results: Aluminium chloride (AlCl3) produced a marked decline in MWM performance and ambulatory
movements' of animals, reflecting impairment of memory and learning. Trans-Sinapic Acid
treatment significantly modulates AlCl3 induced memory deficits, biochemical and pathological alterations.
The findings demonstrate that the memory restorative ability of trans-Sinapic Acid may be
attributed to its anti-cholinesterase, anti-oxidative and anti-inflammatory potential.