Science and Research Questions

Please schedule an appointment for your mother to visit her physician. Your father's passing could have triggered a severe bout of depression in your mother, which could have worsened her memory problems and could also interfere with her sleep patterns. Antidepressants could help in this case. If it is not depression, her doctor may prescribe anti-anxiety medication to help her to relax. In the meantime, make sure her home environment is calm and soothing. Reassure her often that she is safe, loved, and that she will be taken care of in the future. Encourage her to perform some sort of physical activity to the best of her ability each day, even if it is only walking around the room a few times. Regular exercise can facilitate good sleep at night, and may help to reduce her episodes of insomnia. Also, avoid giving her any caffeinated products or alcohol, both of which can interfere with sleep.

The gene, called Apolipoprotein E (ApoE), appears to be a risk factor for the late-onset form of Alzheimer's disease. There are three forms (also known as alleles) of this gene: ApoE2, ApoE3 and ApoE4. Roughly one in four Americans has the ApoE4 gene and one in twenty has ApoE2. While inheritance of ApoE4 increases the risk of developing the late-onset form of Alzheimer's disease, inheritance of ApoE2 substantially protects against the disease.

There is a genetic test that determines which ApoE alleles you are carrying, but it is expensive. You can ask your primary care physician to recommend a genetic counselor and testing facility in your area. However, be aware that even if you were to find out you have the ApoE4 gene, it would only mean that you have a slightly higher risk of developing Alzheimer's disease than the general population. Having the ApoE4 gene does not mean that a person will definitely get Alzheimer's disease. Remember that about a quarter of the population has this gene—the majority of these people never go on to develop Alzheimer's disease. A genetic counselor can explain your specific results in greater detail. In the meantime, keep up the good work with your exercising and try to limit your intake of foods high in trans- or saturated-fats and cholesterol.

Not having a right hemisphere of the brain is not in and of itself a symptom of Alzheimer's disease. In fact, if a person with Alzheimer's disease were to present with only half a brain, that person would undoubtedly be in a very advanced stage of the disease and their missing hemisphere would most likely be due to severe neuronal degeneration. Because the condition you were born with is so rare, there really is no data available as to whether it has any effect on the risk of developing Alzheimer's disease. Similarly, while both adult attention deficit disorder (AADD, also known as ADHD or ADD) and early Alzheimer's disease share similar traits, such as a decreased ability to perform tasks involving focused attention, the two disorders are not related. However, if you are concerned because you or a loved one suspects something is wrong, please talk to your physician.

If you still live in the research triangle area, you can try contacting the neurology or neuroscience departments at your local research institutions, explaining your situation, and asking whether they are recruiting participants for any future Alzheimer's studies. You can also search for Alzheimer's clinical trials in your area that you can participate in under the “Search for Clinical Trials” link in the Resources section of our website.

Scientists still debate whether the inflammatory damage observed in the brains of Alzheimer's patients is a symptom of the disease or a primary cause of it. In any case, the inflammation caused by a vaccination usually occurs locally around the injection site, and would not likely cause inflammation in the brain. And while there is one doctor (Dr. Hugh Fudenberg, M.D.) who reports that the risk of developing Alzheimer’s disease increases if the patient has had five or more consecutive influenza vaccine shots, this study (based on patient records spanning from 1970-1980) has not been repeated or verified. Other doctors have suggested that the mercury preservatives in the flu vaccines are the cause of the increased risk, not the influenza virus itself. However, within the general scientific community there is no conclusive evidence that mercury toxicity or infectious agents such as the influenza virus contribute to the development of Alzheimer’s or any other neurodegenerative disorder.

One study performed over a decade ago in 118 Alzheimer's disease patients and their families found that a subset of 10 families had a significant maternal inheritance pattern. However, according to a study performed in 1999 in over 300 families, there was no cumulative risk of maternal transmission of Alzheimer's disease. In fact, contrary to the researchers’ hypothesis that Alzheimer’s disease may be transmitted maternally, there appeared to be an increased risk of paternal transmission of dementia. Because the results of these and other studies contradict each other, it is difficult to conclude whether a parent’s gender influences disease susceptibility. Additional research on this area would clearly be necessary to make any such determinations.

Niemann Pick Type C disease, a type of lysosomal storage disease, is often referred to as childhood Alzheimer's disease. It is a very rare and fatal genetic disorder in children, and those with NP-C usually do not survive past their teenager years. Because children afflicted with NP-C lack a specific protein critical for the processing and removal of complex lipids (cholesterols called gangliosides) from their nerve cells, the lipids accumulate and eventually kill the neurons. NP-C children display neurological symptoms similar to Alzheimer's disease, such as issues with balance, memory loss, and other cognitive problems. Unfortunately, there are no proven therapies for NP-C, nor is there a cure.

Valproic acid (VPA) is a drug that has been used to treat epilepsy and bipolar disorder. Researchers at Canada’s University of British Columbia in Vancouver recently discovered that VPA reduced and even slightly prevented the buildup of amyloid plaques in the brains of Alzheimer's disease-model mice when given early on in the disease. Mice given the drug also performed better on memory tests compared to mice given a placebo. VPA is thought to work by inhibiting the enzyme that produces beta amyloid, thereby preventing the accumulation of amyloid protein that becomes toxic to neurons. This study, conducted by Dr. Weihong Song, is published in The Journal of Experimental Medicine.

VPA was previously tested in Alzheimer's disease patients to assess for drug tolerability and to see whether it reduced agitation and aggression. These earlier studies did not look at VPA’s effects on brain plaques. Dr. Wong and his team are enthusiastic about the results in mice and think that the same strategy could prove effective in humans. In fact, a small clinical trial testing VPA’s efficacy on early-stage Alzheimer's disease patients is currently underway.