Science and Research Questions

Paranoia and other psychiatric behavior is more often an initial symptom of frontal lobe dementias, such as Pick’s disease, than of dementia caused by Alzheimer's disease.

Psychosis and paranoia can occur in other forms of dementia and in Alzheimer's disease, but usually only after the disease has progressed for some time. For example, because they may no longer be able to rationalize what they see or remember who people are, Alzheimer's patients commonly report that people are stealing from them or that there are strangers in their home. In fact, these patients most likely just forgot where they put their items or do not recognize their own reflections in the mirror.

Interestingly, it has been reported that there is a higher risk for schizophrenic patients (who commonly suffer from paranoia) to develop dementia later in life. Several studies have indicated, for example, that when schizophrenia develops late in life (>60 years), there is a higher likelihood that dementia will also be diagnosed.

Medium-chain triglycerides (MCTs) are quickly metabolized by the body to form ketones (also known as ketone bodies). Normally, the brain uses glucose as a primary source of fuel. Researchers believe that brain cells (neurons) altered by Alzheimer's disease are not able to adequately metabolize glucose and therefore perform more poorly, which can lead to cognitive impairments. MCTs converted to ketones by the liver can therefore serve as an alternative fuel source for neurons, allowing them to function better. Besides Alzheimer's disease, the “ketogenic diet” approach has been investigated as a therapy for a number of neurological and metabolic disorders, including intractable epilepsy and phosphofructokinase deficiency, with positive results.

Two recent clinical studies demonstrated that patients having probable Alzheimer’s disease or mild cognitive impairment (MCI) had improvements in cognition and memory when given a medical food containing MCTs. Researchers believe that the ketogenic diet may actually be neuroprotective, and may therefore be beneficial not only for the treatment of neurodegenerative disease, but also in instances of stroke and brain injury. In addition, one study in animals found that ketones can reduce brain beta-amyloid levels, which if true in humans, may also be very beneficial in the treatment of Alzheimer’s disease.

The usual progress of Alzheimer’s disease is slower than what you’re describing, though there are times when the increase in confusion seems to have increased by leaps and bounds. If someone with dementia seems to get much more confused over the course of a few days, though, it’s a good idea to let his or her primary care clinician know so they can look for acute conditions that may be exacerbating the dementia. Infections, taking a new medication that has side effects, or experiencing the effects of a stroke or other acute medical illness are each factors that could account for a rapid increase in confusion that would be important to assess right away in order to assure optimal treatment.

Sleep talking is sometimes more disruptive and disturbing to others than to the speaker, but justifies some concern particularly if it represents a significant sleep disturbance for your grandfather. It is not a very common symptom of aging or dementia, but sometimes reflects the experience of vivid dreams that is associated with taking donepezil (Aricept). If the sleep talking only began after the Aricept was started, you might ask your grandfather’s prescribing doctor or nurse to consider reducing the dose, moving it to the morning, or perhaps replacing it with a different medication. There are also medications for reducing nightmares if they are present, but their use needs to be monitored closely because of potential side effects. An important but infrequent cause of sleep talking is Rapid Eye Movement Behavior Disorder (RBD), a sleep disorder that is associated with disinhibition of muscle activity during the dream phase of sleep. A person with RBD might talk, walk, or even hit others while dreaming. These motor actions are usually prevented during normal sleep. Since RBD can precede Dementia with Lewy Bodies, a condition with some important differences from Alzheimer's disease, your grandfather's clinician should be informed about the sleep talking.

Alzheimer’s disease is the most common dementia, and accounts for two thirds of the dementia cases among older adults in the United States, but Parkinson’s disease is an important diagnosis among the remaining individuals, since approximately 30% of people affected by this neurological condition will also eventually develop symptoms of dementia.

All dementias are currently defined as including a problem with memory (typically a problem with forming new memories or retrieving recent memories) as well as problems with language, task performance, recognition, or the ability to problem-solve and manage various tasks (called executive function). The cause of the dementias generally involves death or disrupted function of brain cells, but this can happen through a variety of different insults to the brain. In Alzheimer’s disease, an abnormal protein (amyloid-beta) interferes with brain function. In vascular dementia, disruption of oxygen and nutrients to brain cells results from blood vessel disease in the brain, and in Parkinson’s disease the cause may be related to dysfunction in specific groups of brain cells that secrete dopamine, an important brain chemical involved in nerve cell communication.

The full description of the potential causes and underlying abnormal brain processes that lead to the various dementias, as well as other relevant information has occupied many books. An excellent introduction to Alzheimer's disease is called, “Alzheimer's Early Stages,” by Daniel Kuhn, and is published by Hunter House. A more technical book, by Dr. Marc Agronin, is called, “Alzheimer Disease and Other Dementias: A Practical Guide,” and is published by Lippincott Williams & Wilkins. A moving memoir that describes the effects of Parkinson's disease and dementia on the life and career of a prominent physician was published in 2008 by Sterling Publishing Company, and is titled, “Life in the Balance: A Physician's Memoir of Life, Love, and Loss with Parkinson's Disease and Dementia.”

While it is relatively unusual for a person in their early 40s to develop Alzheimer's disease (AD), it is not unheard of. Familial Alzheimer’s disease (FAD) or early-onset Alzheimer's is an inherited, rare form of the disease, affecting less than 10 percent of all AD patients. FAD develops before age 65, in people as young as 35. It is caused by one of three gene mutations on chromosomes 1, 14 and 21.

If, for example, you have one of the three known mutations that are linked to FAD, the two strokes you had could have contributed to hastening the progression of the disease. Stroke causes damage to the brain just as a traumatic head injury might, and this could influence or accelerate any disease process already underway on account of the genetic mutations.

On the other hand, if you do not have the familial form of AD, then your case is quite unique. There are very few instances of persons in their 40s who develop the non-inherited form of AD. Because of your age and the fact that you have had two minor strokes, one possibility is that a congenital condition has contributed to the development of the disease.  Put another way, perhaps a congenital anomaly in the vasculature of your brain has made you more prone to having strokes, and perhaps you have suffered more mini strokes than you are aware. The cumulative effects of the damage caused by numerous mini strokes could have contributed to brain damage and subsequent neurodegeneration over time, which could have made you more prone to developing AD.

Chronic pain (such as low back pain, etc.) has also been associated with brain atrophy (shrinkage), as has carbon monoxide poisoning—both or either of which can obviously occur in persons of any age. However, neither of these conditions have been directly correlated with the development of dementia or Alzheimer's disease.

Of course, all of these possibilities are purely theoretical, as it is impossible to make such a diagnosis without a thorough examination.  If you have not already consulted a neurologist, you may want to consider doing so.

The most commonly affected brain regions include the frontal lobe (which governs social behavior, judgment and reasoning), the hippocampus (memory), and the parietal and temporal lobes (language, motor control).  As the disease progresses, there is an overall shrinkage of brain tissue as the damage to the brain becomes widespread.  Therefore, by the end stages of Alzheimer's disease, all regions of the brain are potentially at risk of damage and degeneration.

Your question raises a number of issues, so I want to begin by reassuring you that I could find no evidence either that your childhood encephalitis or temporal lobectomy are regarded as increasing later risk for Alzheimer's disease. Now let me Address the broader inheritance issues:

Family members who witness the effects of Alzheimer's disease on a loved one cannot help but wonder whether their own futures hold similar fates. Inherited genes, though, are only one of the factors affecting the risk for developing Alzheimer's disease. Genes are most clearly important in determining risk among the small number of Alzheimer's disease cases that develop earlier in adulthood.

Among middle-aged adults who develop Alzheimer's disease, nearly half have inherited genes associated with one of the familial early onset forms of Alzheimer's. With later onset, genes are a less important contributor to risk, even despite occurrence of the illness in both your father and his mother.

One gene in particular, the Apolipoprotein E (ApoE) gene, has been shown to decrease age of onset if not actually increase the risk for occurrence of late onset Alzheimer's Disease. Testing for the ApoE gene is available but most authorities do not recommend routine clinical use of the test. This is because many people with the more risk-related test results never develop Alzheimer's disease yet many with the less risk-related results do develop the disease.

Researchers are currently trying to sort out other genetic factors that may be present in families possessing multiple members with late onset development of Alzheimer's disease.

With greater life expectancy, attention to non-genetic risk factors has become increasingly important, and these factors are most important to address before the later years of life. Diet, weight, physical exercise, and mental activity all seem to be important considerations in reducing the risk for later development of Alzheimer's disease. Limiting the use of alcohol and tobacco and obtaining treatment for medical problems such as high cholesterol, high blood pressure, or diabetes are additional important steps for optimizing cognitive health in the later years.