Science and Research Questions

There have been several studies that have looked at the average survival time following a diagnosis of Alzheimer’s disease. All of the studies basically come to the same conclusion: the median survival time following diagnosis is largely dependent upon the age at which the person was diagnosed and/or disease severity at time of diagnosis. For example, persons diagnosed as having mild AD at age 55-65 had a average survival time of 6-10 year, whereas patients diagnosed in their 70s, 80s or 90s, or patients with more severe dementia symptoms at the time of diagnosis, had a much lower average survival time, sometimes as low as 3 years. Of course, the overall health of the patient at the time of diagnosis and whether or not they have any other disease conditions (heart disease, diabetes, gait disturbances, etc.) also greatly affects survival time following diagnosis. Some studies on this topic include the following articles, which are available through PubMed or through your local medical or research library:

Brookmeyer R, Corrada MM, Curriero FC, Kawas C. Survival following a diagnosis of Alzheimer disease. Archives of Neurology, 2002 Nov; Vol. 59, No. 11, pages 1764-1767.

Larson EB, Shadlen MF, Wang L, McCormick WC, Bowen JD, Teri L, Kukull WA. Survival after initial diagnosis of Alzheimer disease. Annals of Internal Medicine, 2004 Apr; Vol. 140, No. 7, pages 501-509.

Zanetti O, Solerte SB, Cantoni F. Life expectancy in Alzheimer disease (AD). Archives of Gerontology and Geriatrics, 2009; Vol. 49, Suppl. 1, pages 237-243.

Lipogen PS is composed primarily phosphatidylserine, a constituent of biological membranes. Lipogen PS is soy derived but there is no evidence that it is more effective than phosphatidylserine from other sources. These agents have been reported to give modest and temporary improvement to patients with early symptoms of dementia.

There are no recommended and effective dietary treatments for patients with Alzheimer's disease; however, there is good evidence that a balanced diet that contains monosaturated fats (found in the Mediterranean diet) reduces risk of developing this neurodegenerative disease.

There is a considerable body of literature suggesting that modest memory impair can occur in the normal person or animal after general anesthesia. This usually is not debilitating and diminishes in severity over a period of months. Your wife's case is an unusual one in the fact that the decline in her function was so profound. The brain of a demented person has much less "reserve" than that of a normal person of the same age. A drop in blood flow under anesthesia or other effects of the anesthetic on structural proteins of the nerve cell could underlie these changes. The anesthetic does not remain in the system for a prolonged period after surgery so it is unlikely that its effect can be reversed. Without examining your wife, it is extremely difficult to be specific about what has happened and what might be done. I would suggest that she be thoroughly evaluated by a neurologist or other physicians with experience in dementia.

While some studies have suggested that tobacco use (and in particular cigarette smoking) may actually reduce the risk of developing Alzheimer’s disease (AD), more recent studies have found this to be incorrect. Earlier research may have been biased on some factors (for example, the authors conducting the research were affiliated with the tobacco industry). Also, because non-smokers generally live longer than smokers, the occurrence of age-related diseases such as Alzheimer’s disease may be biased to reflect more non-smokers having AD. When these and other factors are taken into account, the most recent evidence indicates that cigarette smoking is indeed a risk factor for AD. Unfortunately, however, these studies were mainly focused on cigarette smoking. None of the research so far has looked into snuff use as a risk factor for Alzheimer’s disease.

Interestingly, nicotine - one of the main chemicals found in tobacco - is known to improve concentration, coordination and short-term memory. Researchers therefore became interested in using nicotine therapeutically, such as for the treatment of neurodegenerative disease. These results are also mixed. Some studies have found that Alzheimer’s patients (or transgenic mouse models of AD) show improvements with chronic nicotine treatment, while other studies have found no beneficial effect. Therefore, more research is clearly needed to determine if nicotine can impact the course or progression of AD.

That being said, could snuff use have influenced your husband’s disease onset or progression? It is quite possible that it did, however, without more research on the effects of smokeless tobacco on neurodegenerative diseases, it is impossible to say just how (positively or negatively) snuff use affected your husband’s disease.

On average, patients with Alzheimer's disease live for 8 to 10 years after diagnosis, and the majority of people who are diagnosed are at least in their mid- to late-sixties. However, this terminal disease can last for as long as 20 years.

On a day to day basis, an Alzheimer’s disease patient’s memory can definitely fluctuate. In extreme cases, one day a patient may know his spouse caregiver, the next day he may think that same person is an intruder in his home. However one thing is consistent: if you were to chart the overall memory capacity of an Alzheimer’s disease patient, you would certainly see a gradual decline over a long period of time (e.g., months or years).

Researchers at Columbia University in New York recently reported that a drug belonging to a class of agents used for treating cancer can improve the memory of transgenic mice that are a model of Alzheimer’s disease (AD).

The drug is a histone deacetylase (HDAC) inhibitor. The researchers noted that transgenic AD mice had lower levels of acetylated histone 4 (called H4) in their brains than wild-type (non-transgenic) mice. Acetylated histone is required for the synthesis (production) of new proteins by brain cells. The researchers believed that the memory impairments observed in AD patients (and in the transgenic AD mice) is due to a defect in the ability of their brain neurons to synthesize new proteins, which is critical for the process of making and retaining memories. The researchers tested their hypothesis by giving an HDAC inhibitor (which blocks the breakdown of acetylated histone, thereby allowing more of it to be available in the brain for protein synthesis) to the AD mice and then testing their memory. The AD mice administered the HDAC inhibitor scored as well as the wild-type (non-diseased) control mice on the memory tests, thus indicating that HDAC inhibitors can improve memory functioning in individuals the animals with impaired memory.

Clearly, the findings of this study have implications for Alzheimer’s disease patients in terms of a potential new therapeutic approach. But it also clear that additional research will have to be performed to validate these results in other animal models and then in humans. One good thing, the drug used in the study has already been approved as safe for human use for the treatment of certain forms of cancer, so that that puts it one step closer to its potential use as a treatment for Alzheimer’s disease.

There is at least one published case report indicating that Demerol® (generic name merperidine) can cause the confusion of dementia to worsen. As an alternative, the study suggested that Percocet should be offered. In general, however, the benefits of managing or reducing pain in dementia patients to improve their quality of life far outweigh any potential side effects the pain medications may produce. When used responsibly and under the supervision of a doctor, pain medications can play a vital role in reducing or managing pain, thus allowing the dementia patient to perform more activities (both assisted and unassisted) and to be more willing to interact socially with others.