Prospective studies and well-analyzed retrospective studies show that smoking increases the risk of developing Alzheimer's (Biomed Pharmacother. 2004 Mar;58(2):95-9. PMID 14992790). The increased risk may be substantial (J Neurol Neurosurg Psychiatry 2000;68:622-626 (May). PMID 10766894). Cigarettes contain many substances in addition to nicotine, and the increased risks incurred by smokers are not to be confused with the controversial possible slowing of the progression of established Alzheimer's disease by administration of pure medical nicotine.

Nutrition and Alzheimer's
Some work is being done to investigate the role of raised levels of homocysteine, and possible nutritional prevention or treatment through taking of foods high in B vitamins and antioxidants to control the levels of homocysteine.

See: Seshadri S, Beiser A, Selhub J, et al. Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. N Engl J Med. 2002 Feb 14;346(7):476-83.

A deficiency of DHA, an omega-3 fatty acid, has also been implicated in Alzheimer's.[9]

Insulin resistance has also been associated with Alzheimer's. Remarkably, genetic epidemiology has revealed that the ApoE4 allele is found at the highest rates in populations that are current or recently were hunter-gatherers, and at the lowest rates in populations that have long been adapted to agriculture. Some have suggested that the ApoE4 gene only contributes to Alzheimer's when it is found in conjunction with a high-carbohydrate diet.

Treatment

There is no cure, although there are drugs which temporarily reduce neurotransmitter degradation and alleviate some of the symptoms of the disease.

Acetylcholinesterase inhibitors
Acetylcholinesterase (AChE) inhibition was thought to be important because there is selective loss of forebrain cholinergic neurons as a result of Alzheimer's. AChE-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain (combatting the loss of ACh caused by the death of the cholinergin neurons). Acetylcholinesterase-inhibitors seemed to modestly moderate symptoms but do not prevent disease progression including cell death.

Examples include:

tacrine - no longer clinically used
donepezil (marketed as Aricept)
galantamine (marketed as Razadyne, formerly Reminyl)
rivastigmine (marketed as Exelon)
Recently, a controversy has erupted about cholinesterase inhibitors because a study by Courtney (2004) in the respected medical journal The Lancet has suggested they are ineffective. The pharmaceutical companies, but also many unbiased clinicians, dispute the findings of the study, based on methodologic grounds.

NMDA antagonists
Recent evidence of the involvement of glutamatergic neuronal excitotoxicity in the aetiology of Alzheimer's disease led to the development and introduction of memantine. Memantine is a novel NMDA receptor antagonist, and has been shown to be moderately clinically efficacious. (Areosa et al., 2004)

Vaccine
There are ongoing tests of an Alzheimer's disease vaccine. This was based on the idea that if you could train the immune system to recognize and attack beta-amyloid plaque, the immune system might reverse deposition of amyloid and thus stop the disease. Initial results in animals were promising. However, when the first vaccines were used in humans, brain inflammation occurred in a small fraction of participants, and the trials were stopped. Participants in the halted trials continued to be followed, and some showed lingering benefits in the form of slower progression of the disease. Recent studies in mice continue to show promise that an approach may be found to avoid the inflammation issue. It is hoped that research will provide a better formulation and that in the future it can be of use in families with history of Alzheimer's disease.

Pure Medical Nicotine
One study indicated that intake of pure medical nicotine might help delay progression of Alzheimer's disease in carriers, but not non-carriers, of the ApoE4 gene. The issue of whether medical nicotine intake may delay Alzheimer's progression among some sub-populations of patients remains a focus of debate. But no one is advocating smoking, as distinct from prescription nicotine, for the treatment or prevention of Alzheimer's. In prospective studies and well-analyzed retrospective studies, smoking is shown to increase the risk of developing Alzheimer's. Biomed Pharmacother. 2004 Mar;58(2):95-9.

Genetic and population effects
Various gene alleles have been associated with Alzheimer's disease, most notably the apolipoprotein E (ApoE) gene. ApoE normally functions to regulate cholesterol metabolism. In addition, it has recently been discovered that Chinese and North American populations differ significantly in development of full-fledged Alzheimer's from early warning symptoms. Whether the reason for this is genetic, dietary, or social has yet to be investigated.

The ApoE4 form of ApoE, which is associated with Alzheimer's, is found at the highest rates among long-time hunter-gatherers, and at the lowest rates among populations who have been accustomed to agriculture the longest. This has led some researchers to suggest that ApoE4, which exerts some of the same effects on metabolism as a diet excessively high in carbohydrates, contributes to Alzheimer's only in conjunction with an evolutionary discordant high-carbohydrate diet. [11]

Social issues
Alzheimer's is considered to be a major public health challenge since the median age of the industrialized world's population is increasing gradually. For this reason, money spent informing the public of available effective prevention methods may yield disproportionate benefits. The role of family caregivers has also become more prominent, as care in the familiar surroundings of home may delay onset of some symptoms and delay or eliminate the need for more professional and costly levels of care.