Alzheimers disease is a primary degenerative disease
of the central nervous system. The progression of Alzheimers disease will
ultimately lead to dementia, behavioral and cognitive impairments. Alzheimers
is the commonest cause of dementia, a group of progressive condition which involves
especially short-term memory loss, poor concentration, poor sense of time and
space, difficulty in finding words or understanding other people, difficulty
in perceiving and interpreting surroundings, mood changes and emotional upsets.
The present study was designed to determine the ameliorating effect of ethanolic
leaf extract of Ficus hispida Linn. (EEFH) on (amyloid beta) Aβ
25-35-induced cognitive deficits and oxidative stress in mice. Animals were
treated with EEFH for periods of 4 weeks dose-dependently (200 and 400 mg kg-1)
then received a single intracerebroventricular (i.c.v.) injection of Aβ
25-35 (10 μg mouse-1). Behavioral changes in the mice were evaluated
using passive avoidance, Y-maze, Hole board and water-maze tests. Anti-oxidant
enzymes and neuro-transmitter levels were also been estimated. EEFH at the dose
of 400 mg kg-1 significantly ameliorated the cognitive and memory
deficits caused by i.c.v. injection of Aβ 25-35. EEFH attenuated the Aβ-induced
increase in brain levels of thiobarbituric acid reactive substances. There was
an increase in glutathione peroxidase, glutathione reductase and super oxide
dismutase activity in EEFH treated groups. The acetyl cholinesterase activity
in the brain was lower in EEFH supplemented groups than the Aβ-injected
group. EEFH treated group showed a significant alteration in behavior when compare
to negative control in Y maze, Plus-maze and also in water maze tests. These
findings suggest EEFH exerts a protective effect against cognitive deficits
induced by Aβ 25-35 accumulation in Alzheimers disease, because of
its potential antioxidant property.
D. Sivaraman, P. Muralidharan and P. Panneerselvam, 2012. Ameliorating Effect of Ethanol Leaf Extract of Ficus hispida Linn.
on Amyloid beta Aβ (25-35) Induced Cognitive Deficits and Oxidative Stress
in Alzheimers Mice. International Journal of Pharmacology, 8: 212-223.