Nicotinic acetylcholine receptors and their interaction with Aβ₁₋₄₂

Alzheimer's Disease (AD) is a progressive, age-related disease that is positively characterised by the post-mortem presence of neurofibrillary tangles and amyloid plaques. At present ~ 5 % of those aged over 65 years are diagnosed with AD, with this figure increasing to ~ 20 % for those aged over 75 years. It is nearly 100 years since AD was first characterised in 1907, however the exact cause has yet to be determined with the cholinergic and beta-amyloid (Ap) hypotheses remaining central to the aetiology. The cholingergic hypothesis suggests that loss of the cholinergic pathways precedes that of any other neurotransmitter making it a primary target in AD and predating the amyloid hypothesis which itself postulates that deposition of Ap is primarily responsible for the neurodegeneration in AD. Until recently, these two hypotheses have been almost exclusively studied in separation. However, recent studies suggest that the two major CNS cholinergic nicotinic acetylcholine receptor subtypes a4p2 and a7 may interact directly with Ap and therefore, a multidisciplinary approach has been used to evaluate the reported interaction.

Grantor dc:publisher

The University of Edinburgh

Year dc:date.issued

2006

Author dc:creator

• Crawford, Nicola

Handle dc:identifier.uri

http://hdl.handle.net/1842/29079

OAI identifier oai:identifier

oai:era.ed.ac.uk:1842/29079