Science and Research Questions

In general, vitamin supplementation can be useful for helping to maintain proper nutrition in an Alzheimer's disease patient, particularly if they are unable to consume a wide range of foods. Vitamin B12 deficiency is actually quite common in the elderly and can cause symptoms of dementia. Overdoses of vitamin B12 are rare, and the vitamin can be safely taken daily. That being said, vitamin B12 works best when it is taken with folic acid (these are often found together in the same vitamin supplement). Also, it is best to give B12 supplements sublingually (i.e., drops given under the tongue) because they are better absorbed and may help to prevent a condition called pernicious anemia, which is basically an anemia caused by the inability to absorb vitamin B12 through the gastrointestinal tract.

There do not appear to be any drug contraindications between vitamin B12 and the most commonly-prescribed Alzheimer’s disease medications, such as Namenda or any of the cholinesterase inhibitors (Razadyne, Exelon, Aricept, or Cognex). However, as I do not know the exact medications your mother is taking, I have no way of knowing if something else may be problematic. It is important to talk with your mother’s physician before giving her any vitamin supplements because they may be contraindicated for certain medical conditions or may react negatively with other medications that are being taken.

There are no studies in the scientific literature or in medical reports indicating that hearing loss contributes to the development of Alzheimer's disease. In fact, in a recent study conducted in China comparing the hearing capabilities of Alzheimer's disease patients and age-matched control subjects, no correlation was found between hearing ability and mental status. It is not uncommon to find both conditions together, however, as both are more common in aged individuals. Nevertheless, hearing loss is not routinely associated with early symptoms of Alzheimer’s disease.

Prior to the German psychiatrist Alois Alzheimer’s first description of the disorder in 1906, the disease was referred to as presenile dementia (or in the case of elderly individuals, senile dementia), or most commonly just dementia.

The emerging field of nanotechnology offers promising new functional approaches to the development of molecular-size solutions to problems in medicine and engineering. In Alzheimer’s research, nanotechnology is being explored as a way to improve diagnostic and therapeutic techniques. For example, scientists have developed a bio-barcode assay that may help in the early diagnosis of Alzheimer’s disease, which would allow patients to seek treatment earlier. Nanotechnology applications may also aid in the treatment of Alzheimer’s disease, such as by providing protection to neurons against oxidative stress, stimulating neuronal growth and repair, and improving therapeutic drug delivery to the brain. However, it is impossible to say for certain whether nanotechnology research alone will eventually lead to an effective therapy for Alzheimer’s disease and an absolute cure for Alzheimer’s disease is still a long way off. More likely, advances in nanotechnology will be used in conjunction with other research techniques to improve existing diagnosis and treatment of Alzheimer’s disease.

Free radicals are highly reactive, unstable molecules that are formed by biochemical reactions within cells, such as by oxidative stress. These molecules seek stability by attacking other molecules (such as DNA and proteins), which can harm cells and tissue and may contribute to the neuronal brain cell damage seen in Alzheimer's disease. One commonly occurring free radical molecule is nitric oxide (NO), which is a reactive oxygen species (ROS). In the healthy brain, ROS are used as signaling molecules that can influence protein production and other cellular functions. For example, animal and tissue studies have revealed that NO acts as a messenger molecule to facilitate memory formation and retrieval. Administration of an antagonist to nitric oxide synthase (NOS, a molecule involved in NO production) was found to block memory formation in laboratory animals.

However, researchers believe that oxidative stress in the Alzheimer's brain leads to the overproduction of reactive oxygen species such as NO. Excessive ROS levels contribute to the disruption of normal brain functioning, leading to the damage and death of neurons. One theory asserts that in the Alzheimer's brain, oxidative damage causes amyloid protein and hyperphosphorylated tau protein to be deposited in an attempt to protect the brain from ROS. Over time, these proteins become the amyloid plaques and neurofibrillary tangles characteristic of Alzheimer's disease. Another theory purports that the amyloid plaques and tau tangles (deposited in response to other factors) cause the oxidative damage, which then leads to the production of ROS and further neuronal damage. There is sort of a “chicken or the egg” dilemma as to which process comes first. Regardless, there is no debate amongst scientists that free radicals are to blame for at least some of the brain damage seen in Alzheimer's disease.

Naltrexone therapy has emerged as a potential treatment for several autoimmune and immune-related diseases, such as Crohn’s disease, multiple sclerosis, and some forms of cancer and lymphoma. At the moment there are only anecdotal reports of low dose naltrexone therapy being used for the treatment of neurodegenerative disease. No formal studies have yet been conducted as to whether this therapy could be an effective treatment for Alzheimer's disease.

Mutations in the presenilin-1 gene (PS1, on chromosome 14), the presenilin-2 gene (PS2, on chromosome 1), and the amyloid precursor protein gene (APP, on chromosome 21) have all been linked to a rare form of early-onset Alzheimer's known as familial Alzheimer's disease (FAD). FAD accounts for less than 10 percent of all Alzheimer's disease cases. At the moment, is only possible to test for the PS1 gene clinically – PS2 and APP genetic testing are currently only performed for research purposes. Even so, tests for PS1 are generally only performed on persons having a family history of FAD, or as an aid to confirm an Alzheimer's diagnosis in persons suspected of having the disease.

If you have a family history of FAD (that is, you have a parent or close relative who developed AD before the age of 65), then you may want to speak to your doctor about the possibly of genetic testing. Your doctor can refer you to a genetic counselor who can take a family history and decide on the best course of action. The genetic counselor may, for example, want to screen for possible PS1 mutations in the affected relative (if he or she is still alive) in addition to screening you. However, please be aware that even if no mutation in your PS1 gene (or your relative's PS1 gene) is found, this does not mean that you will not get Alzheimer's disease (AD). Don't forget that there are the PS2 and APP genes that can still influence disease susceptibility, as well as other genes on other chromosomes. The absence of a PS1 mutation only means that your risk of developing AD (in terms of PS1 genetic susceptibility) is equivalent to that of the general population's risk (that is, it is much lower but it still exists because everyone is potentially at risk for developing AD). A genetic counselor will be able to explain the results of such tests to you in greater detail.

One therapy currently of interest to Alzheimer's researchers involves low level infra-red light (also called low level laser therapy (LLLT)). Infra-red light is believed to help stimulate cell growth and repair, and so it is believed that LLLT may help in cases where neurons are damaged, such as in neurodegenerative disease.

Low level laser therapy (LLLT) has been shown to be effective for the treatment of traumatic brain injury (TBI) in mice. A small device was used to deliver the laser therapy through the skull of the mice (called transcranial delivery). Mice that received LLLT scored significantly better on motor function tests and had smaller areas of brain damage than control mice that did not receive LLLT.

Another group of researchers at the University of North Carolina (UNC) have successfully used LLLT to improve recovery following stroke in human patients. In a small clinical study, stroke patients receiving LLLT had a higher functional recovery score (as measured by the National Institutes of Health Stroke Scale (NIHSS)) – even up to 90 days following treatment – than those who did not receive LLLT. A larger clinical study has been planned.

Such promising results have prompted scientists to ask the question of whether or not LLLT could be used for the treatment of neurodegenerative diseases, such as for Alzheimer's or Parkinson's disease. In fact, a team of British scientists have made a helmet that delivers low level infra-red light (which is able to penetrate through the skin and skull), and which they claim may be able to halt or even reverse some of the symptoms of dementia. However, only one prototype of the helmet exists, and much testing would be required to determine if such a device – or LLLT in general – could be used to treat Alzheimer's disease.