KUMAR3

INTRODUCTION

known for over a century (Dollken, 1897). Increased level of aluminium

has

been

reported

in

the

the

brain

sample

of

patients

with

Alzheimer's

disease

(AD)

and

cholinergic

system

is

severely

affected

in

Alzheimer's disease (Davies and Maloney, 1976). Cholinergic abnormalities

found in AD have not been observed in other mental disorders (Perry and

Perry, 1980). The pathology in the cholinergic cell mass may correlate

better

with

clinical

dementia

than

the

presence

of

neurofibrillary

tangles and senile plaques (McGeer et al.,1984). Aluminium administered

to

experimental

animals

induced

changes

in

the

cholinergic

system

(AChE)

characteristic of AD and also

reduced

the

acetylcholinesterase

activity (Yates et al.,1980). Reduced level of AChE have been documented

in postmortem brain samples of patients with demential disorders (Gulya

et al.,1986). Aluminium has been suggested as a cholinotoxin (Yates et

al.,

1980;

Gulya

et

al.,

1990),

and

the

effect

of

aluminium

on

cholinergic enzyme AChE - a cholinergic marker enzyme - has been reported

to be variable (Meiri et al., 1993). Reports on aluminium induced changes

in AChE activity on chronic exposure are scant. Therefore, the present

study aims to study the changes in AChE activity of rat brain regions on

chronic exposure to aluminium.

The central nervous system is vulnerable to free radical damage and

lipid peroxidation (LPO) can produce changes in the synaptic transmitter

and ion functions (Evans, 1993). Aluminium mediated increase in LPO has