Science and Research Questions

Several studies have attempted to determine whether or not there is a correlation between worsening vision and the development of dementia. For example, some studies have focused on the relationship between either macular degeneration or cataracts and cognitive impairments in elderly patients. Although Alzheimer's disease and age-related macular degeneration may share similar pathology, there does not seem to be an association between cognitive impairment and age-related macular degeneration. That being said, however, there does seem to be an association between certain cataract formations in the eye and Alzheimer's disease. Cataracts are a clouding of the eye lens, which can give the eye a grayish-whitish appearance.

The amyloid beta protein associated with Alzheimer's disease (AD) has been found to be present in the cataracts of both AD patients and non-AD subjects. A team of investigators lead by Dr. Lee Goldstein, however, has discovered that there may be a way to detect Alzheimer's disease in patients with cataracts. The researchers report that cataracts of AD patients were found as an arc around the rim of the lens, which is different from the “normal” cataract occurring in the center of the lens. Dr. Goldstein has developed a test using fluorescence particles injected into the eye and a special light that causes the particles to glow. The fluorescence pattern is then used to determine whether or not the cataracts are indicative of Alzheimer's disease. This work is still in the experimental stages, however, and further research will help determine the whether this strategy could be used for routine diagnosis of AD.

On behalf of its donors, the American Health Assistance Foundation (AHAF) is proud to have funded Dr. Lee Goldstein's project related to this topic, titled "NonInvasive Laser Technology for Alzheimer's Diagnosis."

Neurostin^TM is a non-prescription supplement that is being advertised as being effective in preventing or even reversing memory loss. Although the drug has not itself been tested in any formal clinical trials, its main ingredients (phosphatidylserine, folic acid, vitamins B6 and B12, vinpocetine, L-alpha glycerylphosphorylcholine (alpha-GPC)) have each independently been demonstrated clinically to improve some measure of brain functioning, such as mild improvements in word recall, attention tasks, or other standard cognitive tests.

The various clinical tests also report that the individual ingredients were each well tolerated individually (i.e., they had few negative side effects). In conclusion, there is nothing in the medical or scientific literature to say that the drug Neurostin^TM would not work as claimed; however, there is also nothing in the literature to say that Neurostin^TM will necessarily produce the level of improvement touted by its manufacturer. If you decide to take Neurostin^TM, please first check with your primary care physician before starting it or any other new supplement. Also, please understand that Neurostin^TM may influence only symptoms of the disease and does not impact the underlying causes.

A review of the medical and scientific literature indicates that there is no known association between receiving laser eye therapy and the development of Alzheimer's disease, dementia, or any other neurodegenerative disorder.

There is one case study in which a man who had been diagnosed with Lyme disease later developed Alzheimer's disease. When his brain was autopsied, DNA for Borrelia burgdorferi, the Lyme disease spirochete, was found within Alzheimer's disease amyloid plaques. However, keep in mind that these results are from only one study performed in one person.

Other studies with a larger number of subjects have not found such a connection. For example, one study found no evidence of Borrelia antibodies (antibodies are an indicator that the body has been exposed to a foreign pathogen, which in this case would be the Lyme disease pathogen) in patients with Alzheimer's disease. Clearly, further research needs to be performed in order to determine if spirochetes can in any way influence the development of Alzheimer's disease.

It is known that exposure to lead-based paint can lead to developmental deficits and stunted growth in children. However, now research also shows that lead exposure early in life may also influence Alzheimer's disease-related protein accumulation in the brain. Researchers at the University of Rhode Island found that aged (23 years old) monkeys that were exposed to low levels of lead (Pb) as infants had higher levels of Alzheimer’s disease-related genes, elevated amyloid-beta levels, and greater Alzheimer’s disease-like pathology in their frontal cortex. The researchers thus suggest that exposure to environmental insults during critical brain developmental periods may influence the expression of disease-related genes and gene products (e.g., amyloid-beta protein) later in life.

Bear in mind, however, that this study was performed in monkeys. Although at present there are no studies in humans conclusively linking lead exposure to the development of Alzheimer's disease, based on the studies in monkeys it is not so great a leap to theorize that exposure to lead early in like may increase a person’s risk of developing Alzheimer’s disease. So, is it possible that the environment your mother lived in contributed to her getting dementia? Certainly it is possible, but further research would clearly need to be performed in order to confirm this hypothesis.

Monosodium glutamate (MSG) is a flavor additive commonly used in many processed foods and is also often used in the restaurant industry. In the book “In Bad Taste: The MSG Syndrome,” Dr. George R. Schwartz has theorized that the prevalence of MSG in foods (either as MSG or as hydrolyzed protein additives) may be related to the rising incidence of Alzheimer's disease.

Glutamate at normal physiological levels is fine, and necessary even, because glutamate is one of the brain’s most prevalent excitatory neurotransmitters (i.e., a chemical messenger for brain cells). Dr. Schwartz’s theory is based on the fact that glutamate, in excessive levels, is an excitotoxin. Basically, this means that when neurons (brain cells) are exposed to very high levels of glutamate, they can become over-stimulated and can be damaged or even die. Dr. Schwartz therefore believes that the chronic, long-term exposure to MSG may lead to neuronal cell damage or death, and that this cell death may contribute to the development of neurodegenerative diseases such as Parkinson’s disease or Alzheimer's disease.

Presently, however, there is no scientific evidence to confirm this hypothesis. Currently, there are no studies indicating any association between the consumption of MSG and an elevated risk of dementia or any other neurodegenerative disease. In fact, toxicity studies have indicated that extremely high doses of MSG need to be administered as a bolus dose (i.e., all at one time) in order to cause neural lesions in the hypothalamus (a brain area that is involved, among other things, in salt balance homeostasis). However, only young rodents seemed susceptible to these neural lesions —– older mice, other mammals and most particularly primates were insensitive to the neural-lesioning effects of MSG. And even when large doses of MSG in drinking water was given to human subjects, the blood levels of glutamate in these humans did not even come close the blood plasma levels associated with neural lesions in mice. Further research on the effects of MSG on brain cells obviously would need to be performed before any conclusion can be drawn about its potential to influence the development of dementia.

Memory impairment is one symptom of Alzheimer's disease, but it is also a symptom of a number of other conditions and disorders so it may be premature to think it is Alzheimer's. For example, stress, depression, vitamin B12 deficiency, interactions between medications (or side effects from a new drug), hypothyroidism (low thyroid hormone levels), and even viral infections can all cause memory problems, confusion, and mood swings. Not that having a few drinks here and there means that one has a drinking problem, but if your father imbibed more often than not, that could also affect his memory over the long-term. The excessive, long term abuse of alcohol has been shown, for instance, to contribute to the development of alcohol dementia, also known as Wernicke-Korsakoff's syndrome or alcoholic encephalopathy, which can cause impairments in memory, vision, and gait. The good news is that many of the aforementioned conditions which can cause memory impairments are treatable, but without a thorough doctor's examination it is not possible to diagnose your father or to begin to treat his memory problem

Presenilin-1 (PSEN1) and presenilin-2 (PSEN2) are cellular transmembrane proteins that are involved in amyloid-beta processing. The presenilin proteins form complexes with other proteins, and these complexes (gamma-secretases) function to chop up the amyloid precursor protein (APP) into small protein pieces, such as the amyloid-beta peptide. Mutations in either of the two presenilin genes (PSEN1 or PSEN2) have been linked to cases of early-onset Alzheimer's disease, also known as familial Alzheimer's disease (FAD). Researchers are still trying to determine the mechanism through which mutations in these genes cause the disease. Beta-amyloid is a fragment of a protein that is snipped from its parent protein, amyloid precursor protein (APP).

So what you refer to as “presenilin disease” is actually Alzheimer's disease caused by a mutation in one or both of the two genes. It is an inherited disease and is not contagious. So if your grandfather did “bring something back” from Ireland, it was something that was already present in his genes to be passed on to his descendents, not something he could have contracted while in a psychiatric facility or hospital. The test that was performed on you was probably to look for mutations in the PSEN1 and PSEN2 genes. Your testing negative means that you do not have the presenilin mutations that are associated with the development of FAD.