Abstract form
Title: Nicotinic acetylcholine receptor involvement in Alzheimer's diseasetype pathology
Presenter: Charles Scerri BPharm (Hons) MPhil PhD (Dundee) CBiol MIBiol
Contact address: Laboratory Officer II, Department of Pharmacy, University of Malta.
Tel: 2340 2905
Fax: 21320281
Presentation date: Monday 7th February 2005
(approximately 200-250 words)
Alzheimer's disease (AD) is the most common form of dementia in the elderly. Its pathology
is characterized by the deposition of neuritic plaques composed of amyloid beta (Aβ)
protein, which is derived from the enzymatic cleavage of the larger amyloid precursor
protein (APP), and intracellular neurofibrillary tangles made up of abnormally
phosphorylated forms of the microtubule associated protein tau. Neuronal degeneration with
impaired cholinergic transmission is also present, particularly in areas of the cerebral cortex
and hippocampus. Several studies suggest that nicotine, through its interaction with nicotinic
acetylcholine receptors (nAChRs), is effective in attenuating cognitive deficits associated
with AD. Our results point out to the role of these receptors in both the pathology and
cognitive effects observed in AD. Cholinergic activation by nicotine administration was
found to affect the processing of APP and tau in the hippocampus both in vivo and in vitro.
Chronic nicotine administration was also found to dose-dependently reduce acquisition of a
memory task and cell proliferation and induce apoptosis in the hippocampal dentate gyrus of
rats. These findings provide evidence that nicotine can influence biochemical processes
involved in the pathology of AD and contribute to a more comprehensive understanding on
the role of cholinergic systems in neurodegenerative disorders.