Diet contributes to the development of AD through modulating oxidative stress and inflammation, which is also linked to oxidative stress, but may also arise from series 2 prostaglandins. A positive relationship between caloric, as well as fat, intake and the prevalence of Alzheimer s disease is demonstrated. These findings link Alzheimer s disease to diet in a more general sense than previous studies that focused instead on specific dietary components such as consumption of brain, raw meat, seafood, alcohol, coffee or vitamin supplements. These latter studies usually had the single goal of determining whether food-borne pathogens or toxins might be implicated, rather than focusing on foods as a source of nutrients. Therefore, nicotinic acetylcholine receptors have attracted considerable interest as potential therapeutic targets.
Current approaches aim at the elucidation of molecular changes at all three levels.
Nicotine is widely recognized as an pharmacological agent that facilitates cognitive performance in human smokers as well as preclinical models utilizing rodents or non-human primates. Furthermore, epidemiological studies have consistently shown that the incidence of neurodegenerative diseases such as AD and Parkinson's Disease is lower in cigarette smokers than age-matched controls. These findings have prompted speculation that brain nicotinic receptors could be important therapeutic targets for Alzheimer's Disease. Few studies have controlled for the potential influence of cigarette smoking, which increases the density of nicotinic receptors in human smokers. Therefore, although the findings related to nicotinic receptors and AD to this date are intriguing, they appear to have raised more questions than they have answered.